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1
Naha, K., S. Thakare, G. Vivek, and M. Prabhu. "Adenocarcinoma of lung masquerading as systemic auto-immune disease." Case Reports 2012, jun13 1 (June 14, 2012): bcr0220125822. http://dx.doi.org/10.1136/bcr.02.2012.5822.
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Leslie, R. D. G., and M. Hawa. "Twin Studies in Auto-immune Disease." Acta geneticae medicae et gemellologiae: twin research 43, no. 1-2 (April 1994): 71–81. http://dx.doi.org/10.1017/s000156600000297x.
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AbstractImmune-mediated diseases affect up to 5% of the population and are a major cause of morbidity and mortality. These diseases can be organ specific, such as insulin-dependent diabetes (IDDM) and non-organ specific, such as Rheumatoid Arthritis (RA). Identical and non-identical twins have been used to establish whether these diseases are determined by genetic or environmental factors. The results of these studies have been collated in a new section of the Mendel Institute in Rome.Diseases included in these studies included IDDM, RA, Systemic Lupus Erythematosus (SLE), Multiple Sclerosis (MS) and Myasthenia. Striking differences in concordance rates between identical and non-identical twins in all these studies suggest that genetic factors are important in causing these diseases. All the diseases are known to be associated with HLA genes on chromosome 6 which may account for some or all of the genetic susceptibility. However, in the majority of pairs the affected twin has an unaffected co-twin. These observations suggest that non-genetically determined factors, probably environmental factors and not somatic mutations, are critical. The study of unaffected co-twins, who are at high disease-risk, has allowed the identification of changes which precede and predict the clinical disease. The immune-mediated destruction in many of these diseases is probably caused by T-lymphocytes. Twin studies have shown the importance of genetic factors in determining T-cell responses. Identical twins should, therefore, provide the perfect test bed to assess the role of T-cells in immune-mediated diseases.
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Chen, Yunying, Fredrik Wermeling, Sven Petersen, Ylva Kaiser, and Mikael Karlsson. "Memory to self-antigens in Systemic Lupus Erythematosus (P4020)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 42.11. http://dx.doi.org/10.4049/jimmunol.190.supp.42.11.
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Abstract Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease associated with auto-IgG antibodies, which are produced due to defective clearance of apoptotic cells (AC) and loss of tolerance to self-antigens. SLE follows flare and remission courses; disease symptoms can come rapidly and unpredictably, suggesting the presence of immune memory to self-antigens in patients. However, experimental evidence and molecular mechanisms behind this are not known. We set up a mouse model by injecting normal mice with syngenic AC weekly for 4 weeks that breaks tolerance and induces auto-IgG production. One month later the serum auto-IgG drops to pre-immune level, these mice can rapidly respond to a single AC injection and produce increased auto-IgGs. This memory-like response is transferable into naïve mice. Serum level of auto-IgG subclass IgG2, but not IgG1, is dramatically increased in the memory response compared to that in the primary response, which contribute to pathogenic effects. The memory auto-IgGs are produced via both germinal center and plasmablast pathways. Spectratyping shows that B-cell repertoire is more skewed in memory response than that in pre-immune and primary response. These observations demonstrate an inducible immune memory to self-antigen in normal mice and establish a model for study of SLE flare-like response in mice. In addition, this study suggests that the formation of immune memory to self-antigens contributes to the disease relapse in SLE patients.
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J.P, Pramod. "Decoding the Mysteries of Auto-Immune Disorders." International Journal for Research in Applied Science and Engineering Technology 12, no. 8 (August 31, 2024): 1366–71. http://dx.doi.org/10.22214/ijraset.2024.64123.
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An autoimmune disease (AI) happens when the immune system doesn’t recognise its cells. This leads to a problem with how it reacts to these cells. Some of these diseases can be due to your genes, the environment, or even certain infections. They can affect specific organs or the whole body. Examples of autoimmune diseases are insulin-dependent diabetes mellitus, rheumatoid arthritis, systemic lupus erythematosus, scleroderma, thyroiditis, and multiple sclerosis. But wait—there's more! Other conditions like arteriosclerosis, inflammatory bowel disease, schizophrenia, & some types of infertility also fall into this category. Around 3% of people in North America & Europe have autoimmune disorders. About three out of four people affected are women. How our immune system works and maintains tolerance is a wonder. The present paper aims to explore autoimmune diseases and what causes the immune system to react in a specific way
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Hsu, Eugene, and Manishi Desai. "Glaucoma and Systemic Disease." Life 13, no. 4 (April 15, 2023): 1018. http://dx.doi.org/10.3390/life13041018.
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Glaucoma is the leading cause of irreversible blindness in the world. Due to its potential to cause permanent vision loss, it is important to understand how systemic conditions and their respective treatments can be associated with or increase the risk for developing glaucoma. In this review, we examined the literature for up-to-date discussions and provided commentary on glaucoma, its pathophysiology, and associated risk factors. We discuss systemic diseases and the impact, risk, and mechanism for developing glaucoma, including pharmacologically induced glaucoma; inflammatory and auto-immune conditions; infectious, dermatologic, cardiovascular, pulmonary, renal, urologic, neurologic, psychiatric and systemic malignancies: intraocular tumors; as well as pediatric, and genetic conditions. The goal of our discussion of systemic conditions including their commonality, mechanisms, treatments, and associations with developing glaucoma is to emphasize the importance of ocular examinations and follow-up with the multidisciplinary teams involved in the care of each patient to prevent unnecessary vision-loss.
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Kamiya, Koji, Megumi Kishimoto, Junichi Sugai, Mayumi Komine, and Mamitaro Ohtsuki. "Risk Factors for the Development of Psoriasis." International Journal of Molecular Sciences 20, no. 18 (September 5, 2019): 4347. http://dx.doi.org/10.3390/ijms20184347.
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Psoriasis is an immune-mediated genetic skin disease. The underlying pathomechanisms involve complex interaction between the innate and adaptive immune system. T cells interact with dendritic cells, macrophages, and keratinocytes, which can be mediated by their secreted cytokines. In the past decade, biologics targeting tumor necrosis factor-α, interleukin (IL)-23, and IL-17 have been developed and approved for the treatment of psoriasis. These biologics have dramatically changed the treatment and management of psoriasis. In contrast, various triggering factors can elicit the disease in genetically predisposed individuals. Recent studies suggest that the exacerbation of psoriasis can lead to systemic inflammation and cardiovascular comorbidity. In addition, psoriasis may be associated with other auto-inflammatory and auto-immune diseases. In this review, we summarize the risk factors, which can be divided into two groups (namely, extrinsic and intrinsic risk factors), responsible for the onset and exacerbation of psoriasis in order to facilitate its prevention.
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Bird, Anna Kathleen, Javier Rangel-Moreno, Nida Meednu, Jennifer Hossler, and Jennifer Anolik. "Neutrophils modulate the progression of B cell auto-reactivity in systemic lupus erythematosus." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 117.3. http://dx.doi.org/10.4049/jimmunol.196.supp.117.3.
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Abstract The central feature of systemic lupus erythematosus (SLE) pathogenesis is loss of immunologic self-tolerance. Here, we address a current controversy regarding whether neutrophils influence the development of B cell auto-reactivity SLE. While both human and murine lupus neutrophils produce factors known to fuel adaptive immune dysregulation, including type I interferon, B cell survival factors, and extracellular traps (a putative source of self-antigen), some studies have contended that neutrophils in peripheral lymphoid organs (PLO) suppress B cell activation and differentiation. In order to ask whether neutrophils exert regulatory or deleterious effects on loss of B cell self-tolerance and immune activation, we compare changes in SLE progression following neutrophil depletion in the NZB/W lupus model, either during or after establishment of disease. Following depletion early in disease, we observe pronounced acceleration of proteinuria, anti-dsDNA titers, and germinal center formation. However, neutrophil depletion after onset of overt disease pathology (including proteinuria) does not strongly alter SLE progression, implicating neutrophils as playing a protective role only apparent during disease onset. To elucidate the specific mechanisms underlying neutrophil effects on B cell auto-reactivity, we examine the cytokine profile of neutrophils in direct proximity to B cells in PLO during several stages of disease. With progression of disease, we observe an influx of interferon-alpha-producing neutrophils in direct proximity to B cells in PLO. These data delineate a shifting balance of both regulatory and activating roles for neutrophils in auto-reactive B cell activation/proliferation during SLE progression.
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Hossain, Md Ismail, Shah Md Sarwer Jahan, Md Ashraful Haque, ABM Mobasher Alam, Mainuddin Ahmed, and Md Zakir Hossain. "Systemic lupus erythematosus in male: two case reports." Bangladesh Journal of Medicine 24, no. 2 (August 27, 2014): 82–85. http://dx.doi.org/10.3329/bjmed.v24i2.20222.
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Systemic lupus erythematosus (SLE) is the most common multisystem connective tissue disease. Around 90% of affected individuals are women, with peak onset in the second and third decades. Tissues of all system are damaged by pathogenic auto-antibodies and immune complexes. We report here two cases of SLE in male patient, presented with typical features of SLE. Though the disease is rare in male, but such type of manifestations should be investigated properly to exclude SLE. DOI: http://dx.doi.org/10.3329/bjmed.v24i2.20222 Bangladesh J Medicine 2013; 24 : 82-85
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Yang, Yening. "The comparison between different therapies of Systemic Lupus Erythematosus." Theoretical and Natural Science 49, no. 1 (November 15, 2024): 9–15. http://dx.doi.org/10.54254/2753-8818/49/20241257.
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Abstract. The immune system has three basic functions: defense, surveillance and homeostasis. It helps us monitoring and timely eliminate mutant cells and distinguishing between alien components to maintain self-stability. However, once it loses these abilities, it could cause the autoimmune disease. In this article, I mainly discuss about the Systemic Lupus Erythematosus (SLE), a type of autoimmune diseases which is mediated by type hypersensitivity. SLE patients suffer from chronic inflammatory responses, leading to tissue damage and organ dysfunction. Therefore, purpose of therapeutic schedule is to inhibit the overactive immune system and relieve the inflammatory response. Nowadays, there are three major therapies: Glucocorticoids (GC), immunosuppression agents and belimumab. Glucocorticoids suppresses inflammatory responses and generate anti-inflammatory factors. Immunosuppression agents can not only control SLE and raise the survival rate of long-term prognosis for SLE patients. Belimumab inhibits the survival of B cells by obstructing the interaction between soluble B cell activating factor (BAFF or BLys) and receptors on B cells. This action promotes the apoptosis of auto-reactive B cells, leading to a decrease in auto-antibodies present in the serum. With the development of biotechnology, more and more advanced treatments have emerged and brings new hope to SLE patients.
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Hudspeth, Kelly L., Wang Shu, Jingya Wang, Saifur Rahman, Michael A. Smith, Kerry Anne Casey, Geoffrey L. Stephens, et al. "NK cell phenotype and proliferation in Systemic Lupus Erythematosus." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 194.5. http://dx.doi.org/10.4049/jimmunol.196.supp.194.5.
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Abstract Systemic Lupus Erythematosus (SLE) is a complex autoimmune disorder whose pathology appears to involve many immune cell types. While it is clear that autoantibody producing B cells as well as CD4+ T cell help are key contributors to disease, little is known regarding the role of innate lymphoid cells such as Natural Killer (NK) cells in the pathogenesis of SLE. We have characterized the phenotype of NK cells by multicolor flow cytometry in a large cohort of SLE patients. While the overall percentage of NK cells was similar or slightly decreased compared to healthy controls, a subset of patients displayed a high frequency of NK cells expressing the proliferation marker, Ki-67, which was not found in healthy donors. Only a moderate increase of Ki-67 was observed on other immune cell types such as total CD4+, CD8+ T cells or CD19+ B cells in the same donors. Increased NK cell proliferation was found to correlate with clinical parameters. Furthermore, proteomics analysis and auto-antibody arrays revealed significant correlations between NK cell expression of Ki-67 and specific serum protein biomarkers, as well as SLE associated auto-antibodies. These results will contribute to the understanding of the mechanistic role of NK cells in immune-mediated pathology of SLE.
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Jindam, Shashank, Pranav Koraseeka, Suvarna Addagarla, and Ramya B. P. Gelly. "A role of biomarkers in systemic lupus erythematous: a comprehensive review." International Journal of Basic & Clinical Pharmacology 11, no. 3 (April 22, 2022): 271. http://dx.doi.org/10.18203/2319-2003.ijbcp20221044.
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Systemic lupus erythematous (SLE) is an auto immune disease that can involve almost all body organs. Lupus erythematous may be classified in to several subtypes according to clinical features including systemic and cutaneous lupus erythematous, drug induced lupus and neonatal lupus. SLE progression includes in the immune system. Pathological manifestation of SLE are due to antibody formation and deposition of immune complexes in different organs of the body. Due to formation or disposition of immune complex in different body tissues and vessels, which may lead to complement activation and more organ damage. Other factors include genetic factors, hormonal abnormalities and environmental factors. There is a challenge in establishing a diagnosis, determining disease activity. Therefore, an important needs is a repertoire of biomarkers that can accurately with prediction, diagnosis, and disease, activity monitoring and stratifying patient. SLE can be diagnosed by using different biomarkers as anti-smith antibodies (ANAS), antibodies to double stand deoxyribonucleic acid (DNA) and level of complement components C3 C4, and CH50. More immunological biomarkers are needed to be better understanding of disease SLE. SLE is an autoimmune disease which can travel to any organ or a system i.e. biomarkers for cardiovascular involvement in SLE, biomarkers for respiratory involvement in SLE, biomarkers for lupus arthritis.
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Bal, Mehmet V., Cenker Z. Koyuncuoglu, and Işıl Saygun. "Immune Thrombocytopenic Purpura Presenting as Unprovoked Gingival Hemorrhage: a Case Report." Open Dentistry Journal 8, no. 1 (September 29, 2014): 164–67. http://dx.doi.org/10.2174/1874210601408010164.
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Immune thrombocytopenic purpura is an autoimmune disease characterized by auto-antibody induced platelet destruction and reduced platelet production, leading to low blood platelet count. In this case report, the clinical diagnose of a patient with immune thrombocytopenic purpura and spontaneous gingival hemorrhage by a dentist is presented. The patient did not have any systemic disease that would cause any spontaneous hemorrhage. The patient was referred to a hematologist urgently and her thrombocyte number was found to be 2000/μL. Other test results were in normal range and immune thrombocytopenic purpura diagnose was verified. Then hematological treatment was performed and patient’s health improved without further problems. Hematologic diseases like immune thrombocytopenic purpura, in some cases may appear firstly in the oral cavity and dentists must be conscious of unexplained gingival hemorrhage. In addition, the dental treatment of immune thrombocytopenic purpura patients must be planned with a hematologist.
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Zhao, Lin-Pierre, Berenice Schell, Marie Sébert, Rathana Kim, Pierre Lemaire, Maxime Boy, Stephanie Mathis, et al. "Prevalence of UBA1 mutations in MDS/CMML patients with systemic inflammatory and auto-immune disease." Leukemia 35, no. 9 (August 3, 2021): 2731–33. http://dx.doi.org/10.1038/s41375-021-01353-8.
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Fox, R., M. S. Mills, and J. D. Hutton. "Obstetric case reports: Auto-immune thyroid disease complicating a pregnancy associated with systemic lupus erythematosus." Journal of Obstetrics and Gynaecology 12, no. 5 (January 1992): 309–10. http://dx.doi.org/10.3109/01443619209015513.
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Kanemaru, Mineo, Chiharu Kawamura, Aki Chizuka, Rie Kojima, and Takamasa Nozaki. "Systemic Lupus Erythematosus with Warm-Type Auto Immune Hemolytic Anemia Preceded by Cold Agglutinin Disease." Journal of Nihon University Medical Association 78, no. 3 (June 1, 2019): 151–56. http://dx.doi.org/10.4264/numa.78.3_151.
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Sica, Antonello, Beniamino Casale, Alessandro Spada, Maria Teresa Di Dato, Caterina Sagnelli, Armando Calogero, Pietro Buonavolontà, et al. "Differential diagnosis: retroperitoneal fibrosis and oncological diseases." Open Medicine 15, no. 1 (December 26, 2019): 22–26. http://dx.doi.org/10.1515/med-2020-0005.
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AbstractRetroperitoneal fibrosis is a connective disease of the auto-inflammatory/auto-immune type of the retroperitoneum with unknown etiology and pathological mechanism. The manifestations of the pathology can be local or systemic. Amongst the local symptoms, the dull and constant pain in the hips, back or abdomen is the most frequent.We report here a case of a 47-year-old woman, whose pathogenic mechanism could be related to an “IgG4-related disease” disorder as suggested by an increased serum level of this subclass of IgG and the positive immunohistochemistry.The diagnosis is not easy, because this pathology generates masses; adenomegalies with retro peritoneal development, that makes it similar to lymphomas or metastases from ovarian tumors.
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Jachiet, Vincent, Pierre Fenaux, Anna Sevoyan, Yervand Hakobyan, Lionel Ades, Olivier Fain, and Arsène Mekinian. "Inflammatory and Immune Disorders Associated with Myelodysplastic Syndromes." Hemato 2, no. 2 (May 24, 2021): 329–46. http://dx.doi.org/10.3390/hemato2020019.
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Systemic auto-inflammatory or autoimmune diseases (SIADs) develop in up to a quarter of patients with myelodysplastic syndromes (MDS) or chronic myelomonocytic leukemia (CMML). With or without the occurrence of SIADs, the distribution of MDS subtypes and the international or CMML-specific prognostic scoring systems have been similar between MDS/CMML patients. Moreover, various SIADs have been described in association with MDS, ranging from limited clinical manifestations to systemic diseases affecting multiple organs. Defined clinical entities including systemic vasculitis, connective tissue diseases, inflammatory arthritis and neutrophilic diseases are frequently reported; however, unclassified or isolated organ impairment can also be seen. Although the presence of SIADs does not impact the overall survival nor disease progression to acute myeloid leukemia, they can help with avoiding steroid dependence and make associated adverse events of immunosuppressive drugs challenging. While therapies using steroids and immunosuppressive treatment remain the backbone of first-line treatment, increasing evidence suggests that MDS specific therapy (hypomethylating agents) and sparing steroids may be effective in treating such complications based on their immunomodulatory effect. The aim of this review was to analyze the epidemiological, pathophysiological, clinical and therapeutic factors of systemic inflammatory and immune disorders associated with MDS.
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Islam, Quazi Tarikul, and M. Robed Amin. "Hypovitaminosis D in Adult - A systemic Review." Bangladesh Journal of Medicine 28, no. 1 (March 16, 2017): 34–40. http://dx.doi.org/10.3329/bjmed.v28i1.31900.
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Background: Hypovitaminosis D is now recognized as a pandemic . Vitamin D can be supplied from the dietary sources but is mainly generated endogenously from skin exposure to sunlight via the epidermis, which is the main source of vitamin D synthesis. Despite abundant sunshine,there is high prevalence of hypovitaminosis D in south-east asia and middle east leading to different clinical manifestation including musculoskeletal disorders such as non specific muscle pain, poor muscle strength and low BMD as well as non-musculoskeletal disorders such as increased risk of respiratory tract infections, diabetes mellitus, cardiovascular diseases, auto-immune disorder and cancer. There are multiple factors contributing to the hypovitaminosis D such as extreme of age, female sex, lack of sun exposure, covered clothing style, sunscreen use, skin pigmentation or dark skin, winter season, latitude, malabsorption, anticovulsant drugs, chronic kidney disease, liver disease and obesity.Objectives: To aware doctors, patients, food producers and consumers.Data source: Online search via Google, 101 articles were down loaded, 69 valid papers were selected. Only 17 full text articles were eligible for review.Bangladesh J Medicine Jan 2017; 28(1) : 34-40
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Mejri, Islam, Lenda Ben Hmida, Maroua Kacem, Mariem Msalmani, Houda Snène, Hana Blibech, Aida Ayadi, Jamel Zaouali, and Zied Moatemri. "Case Report: The first reported case of pulmonary alveolar proteinosis with myasthenia gravis in a 27-year-old patient." F1000Research 11 (August 21, 2023): 1439. http://dx.doi.org/10.12688/f1000research.127299.2.
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Background: Pulmonary alveolar proteinosis (PAP) is a very rare diffuse lung disease characterized by the accumulation of amorphous and periodic acid Schiff-positive lipoproteinaceous material in the alveolar spaces due to impaired surfactant clearance by alveolar macrophages. Three main types were identified: Autoimmune, secondary and congenital. PAP has been previously reported to be associated with several systemic auto-immune diseases. Accordingly, we present the first case report of PAP associated with myasthenia gravis. Case: A 27-year-old female patient, ex-smoker, developed a dyspnea on exertion in 2020. The chest X-ray detected diffuse symmetric alveolar opacities. Pulmonary infection was ruled out, particularly Coronavirus disease 2019. The chest scan revealed the “crazy paving” pattern. The bronchoalveolar lavage showed a rosy liquid with granular acellular eosinophilic material Periodic acid-Schiff positive. According to the lung biopsy results, she was diagnosed with PAP. The granulocyte macrophage colony-stimulating factor autoantibodies were negative. Nine months later, she was diagnosed with bulbar seronegative myasthenia gravis, confirmed with the electroneuromyography with repetitive nerve stimulation showing significant amplitude decrement of the trapezius and spinal muscles. She was treated with pyridostigmine, oral corticosteroids and azathioprine. Given the worsening respiratory condition of the patient, a bilateral whole lung lavage was performed with a partial resolution of symptoms. Thus, this previously unreported association was treated successfully with rituximab, including improvement of dyspnea, diplopia and muscle fatigability at six months of follow-up. Conclusions: This case emphasizes on the possible association of auto-immune disease to PAP, which could worsen the disease course, as the specific treatment does not exist yet. Hence, further studies are needed to establish clear-cut guidelines for PAP management, particularly when associated to auto-immune diseases.
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Jovanovic, Vojislav, Amanda Ng Ai Poh, Eliza Ho Xin Pei, Yan Ting Lim, Nurhuda Abdul Aziz, Eoin McKinney, Paul Lyons, et al. "Anti-lipid response in Systemic Lupus Erythematosus (44.4)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 44.4. http://dx.doi.org/10.4049/jimmunol.186.supp.44.4.
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Abstract Systemic Lupus Erythematosus (SLE) is a chronic, multisystem, autoimmune disorder with a broad range of clinical presentations. One of the main factors, proposed to contribute to the development of clinical manifestations of SLE is accumulation and impaired clearance of immune complexes. The aim of the present study was to investigate lipid and anti-lipid antibody profiles in SLE patients’ plasma using ELISA and gas chromatography-mass spectrometry (GC-MS). The SLE cohort employed in this study is composed of 24 subjects and disease monitoring was undertaken with serial BILAG disease scoring. The blood was collected at three time points: at the moment of flare; and 3-months/12-months after treatment had started. For oxysterols (7α-hydroxycholesterol, 7β-hydroxycholesterol, 7-ketocholesterol) we report a trend where lipid levels and corresponding anti-lipid IgG concentrations are significantly reduced during the course of treatment. For phospholipids (oxidized phosphatidylcholine, cardiolipin) we also show high levels of anti-lipid IgG during flare or active disease. Using GC-MS and ELISA we have confirmed an association of high lipid levels and high anti-lipid IgG level with disease flare in comparison to 12 months after the commencement of treatment. We propose that auto anti-lipid IgGs should now be considered a component of the accumulated immune complexes in SLE and thus may contribute to disease pathogenesis.
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Wu, Kevin Y., Merve Kulbay, Cristina Tanasescu, Belinda Jiao, Bich H. Nguyen, and Simon D. Tran. "An Overview of the Dry Eye Disease in Sjögren’s Syndrome Using Our Current Molecular Understanding." International Journal of Molecular Sciences 24, no. 2 (January 13, 2023): 1580. http://dx.doi.org/10.3390/ijms24021580.
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Sjögren’s syndrome is a chronic and insidious auto-immune disease characterized by lymphocyte infiltration of exocrine glands. The patients typically present with ocular surface diseases related to dry eye and other systemic manifestations. However, due to the high prevalence of dry eye disease and the lack of objective and clinically reliable diagnostic tools, discriminating Sjögren’s syndrome dry eye (SSDE) from non-Sjögren’s syndrome dry eye (NSSDE) remains a challenge for clinicians. Diagnosing SS is important to improve the quality of life of patients through timely referral for systemic workups, as SS is associated with serious systemic complications such as lymphoma and other autoimmune diseases. The purpose of this article is to describe the current molecular understanding of Sjögren’s syndrome and its implications for novel diagnostic modalities on the horizon. A literature review of the pre-clinical and clinical studies published between 2016 and 2022 was conducted. The SSDE pathophysiology and immunology pathways have become better understood in recent years. Novel diagnostic modalities, such as tear and saliva proteomics as well as exosomal biomarkers, provide hope on the horizon.
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Singh, B. K., and S. Singh. "Systemic lupus erythematosus and infections." Reumatismo 72, no. 3 (November 19, 2020): 154–69. http://dx.doi.org/10.4081/reumatismo.2020.1303.
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Systemic lupus erythematosus (SLE) is an inflammatory and multi-systemic autoimmune disorder, characterized by an uncontrolled auto-reactivity of B and T lymphocytes, leading to the production of autoantibodies against self-directed antigens and tissue damage. The life expectancy in patients with SLE has improved tremendously in the last two decades, but the mortality rates still remain three times greater compared to those of the general population. Despite increased awareness and improved management, infections remain a major source of morbidity, mortality, hospitalization, and death in patients with SLE. The infections in SLE patients widely range from opportunistic to common bacterial and viral infections with typical or atypical presentations. Moreover, SLE patients exhibit an increased susceptibility to hospital-acquired infections. Factors associated with increased risk of infections include high disease activity, specific immune dysregulation, drug-induced immune deficiency, and organ failure with irreversible damage. Furthermore, immunosuppressive agents may make patients more susceptible to opportunistic infections. A big challenge faced by physicians in these patients is to distinguish between infections and flares of SLE, as infections may mimic them, leading to predicament in diagnosis and appropriate management. Immunosuppression used to treat severe flares of lupus can have catastrophic complications in patients with active infections. There is an urgent need for biomarkers to make an accurate differential diagnosis in this situation. In spite of increased understanding of SLE, many questions remain unanswered. Further research is needed to determine specific immune dysregulation underlying the increased susceptibility to specific infections, predictors of infection in SLE such as genetic markers, and biomarkers that discriminate between disease activity and active infections. Also, measures must be evaluated appropriately to prevent infections, and their complications in SLE.
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Doglio, M., A. Ugolini, B. Camisa, C. Toma, R. Norata, S. Del Rosso, F. Ciceri, et al. "POS1432 CAR-TREGS FOR SYSTEMIC LUPUS ERYTHEMATOSUS." Annals of the Rheumatic Diseases 82, Suppl 1 (May 30, 2023): 1070.2–1070. http://dx.doi.org/10.1136/annrheumdis-2023-eular.5527.
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BackgroundSystemic Lupus Erythematosus (SLE) is an autoimmune disease characterized by an abnormal inflammatory response against nuclear antigens with consequent tissue damage. Autoreactive B cells and auto-antibodies have a fundamental role in SLE pathogenesis. Regulatory T cells (Tregs) physiologically maintain the immune tolerance and are impaired in SLE. Polyclonal Treg trnasfer obtained unsatisfactory results due to the low number of disease-relevant antigen-specific cells. Chimeric Antigen Receptors (CARs) are molecules capable of redirecting T cell specificity. CAR-Tregs proved effective in pre-clinical mouse models of autoimmunity.ObjectivesWe aimed at developing a CAR-Treg based product to be employed in SLE.MethodsWe isolated Tregs from Healthy Donors Peripheral Blood Mononuclear Cells (PBMCs) and expanded them with IL-2 and rapamycin. We transduced Tregs with a Lentiviral Vector encoding for a second-generation anti-CD19 CAR, considering the relevant role of autoreactive B cells and autoantibodies in SLE.ResultsEngineered cells retained their immune suppressive capabilities upon polyclonal stimulation. Noticeably, they acquired new antigen-specific suppressive capacities, being able to block autologous B cell proliferation. We set up a humanized mouse model of SLE. In vivo, CAR-Tregs delayed the occurrence of B cell lymphopenia, producing immunomodulatory cytokines and without showing toxicity or reprogramming towards Th17 pro-inflammatory cells. In inflamed organs, CAR-Tregs restored the normal composition of the immune system.ConclusionIn conclusion, we efficiently generated anti-CD19 CAR-Tregs and proved their efficacy both in vitro and in an in vivo humanized mouse model of lupus.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsNone Declared.
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Ben Hmida, Lenda, Islam Mejri, Maroua Kacem, Mariem Msalmani, Hana Blibech, Houda Snène, Aida Ayadi, Jamel Zaouali, and Zied Moatemri. "Case Report: The first reported case of pulmonary alveolar proteinosis with myasthenia gravis in a 27-year-old patient." F1000Research 11 (December 6, 2022): 1439. http://dx.doi.org/10.12688/f1000research.127299.1.
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Background: Pulmonary alveolar proteinosis is a very rare diffuse lung disease characterized by the accumulation of amorphous and periodic acid Schiff-positive lipoproteinaceous material in the alveolar spaces due to impaired surfactant clearance by alveolar macrophages. Three main types were identified: Autoimmune, secondary and congenital. Pulmonary alveolar proteinosis has been previously reported to be associated with several systemic auto-immune diseases. Accordingly, we present the first case report of pulmonary alveolar proteinosis associated with myasthenia gravis. Case: A 27-year-old female patient, ex-smoker, developed a dyspnea on exertion in 2020. The chest X-ray detected diffuse symmetric alveolar opacities. Pulmonary infection was ruled out, particularly COVID-19 infection. The chest scan revealed the “crazy paving” pattern. The bronchoalveolar lavage showed a rosy liquid with granular acellular eosinophilic material Periodic acid-Schiff positive. According to the lung biopsy results, she was diagnosed with pulmonary alveolar proteinosis. The granulocyte macrophage colony-stimulating factor autoantibodies were negative. Nine months later, she was diagnosed with bulbar seronegative myasthenia gravis, confirmed with the electroneuromyography with repetitive nerve stimulation showing significant amplitude decrement of the trapezius and spinal muscles. She was treated with pyridostigmine, oral corticosteroids and azathioprine. Given the worsening respiratory condition of the patient, a bilateral whole lung lavage was performed with a partial resolution of symptoms. Thus, this previously unreported association was treated successfully with rituximab, including improvement of dyspnea, diplopia and muscle fatigability at six months of follow-up. Conclusions: This case emphasizes on the possible association of auto-immune disease to PAP, which could worsen the disease course, as the specific treatment does not exist yet. Hence, further studies are needed to establish clear-cut guidelines for PAP management, particularly when associated to auto-immune diseases.
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Shobha, Vineeta, Anu Mohan, AV Malini, Puneet Chopra, Preethi Karunanithi, Siva Subramani Thulasingam, Sabariya Selvam, et al. "Identification and stratification of systemic lupus erythematosus patients into two transcriptionally distinct clusters based on IFN-I signature." Lupus 30, no. 5 (January 26, 2021): 762–74. http://dx.doi.org/10.1177/0961203321990107.
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Objective Despite the significant advancement in the understanding of the pathophysiology of systemic lupus erythematosus (SLE) variable clinical response to newer therapies remain a major concern, especially for patients with lupus nephritis and neuropsychiatric systemic lupus erythematosus (NPSLE). We performed this study with an objective to comprehensively characterize Indian SLE patients with renal and neuropsychiatric manifestation with respect to their gene signature, cytokine profile and immune cell phenotypes. Methods We characterized 68 Indian SLE subjects with diverse clinical profiles and disease activity and tried to identify differentially expressed genes and enriched pathways. To understand the temporal profile, same patients were followed at 6 and 12-months intervals. Additionally, auto-antibody profile, levels of various chemokines, cytokines and the proportion of different immune cells and their activation status were captured in these subjects. Results Multiple IFN-related pathways were enriched with significant increase in IFN-I gene signature in SLE patients as compared to normal healthy volunteers (NHV). We identified two transcriptionally distinct clusters within the same cohort of SLE patients with differential immune cell activation status, auto-antibody as well as plasma chemokines and cytokines profile. Conclusions Identification of two distinct clusters of patients based on IFN-I signature provided new insights into the heterogeneity of underlying disease pathogenesis of Indian SLE cohort. Importantly, patient within those clusters retain their distinct expression dynamics of IFN-I signature over the time course of one year despite change in disease activity. This study will guide clinicians and researchers while designing future clinical trials on Indian SLE cohort.
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Afrashteh Nour, Mina, Farid Ghorbaninezhad, Zahra Asadzadeh, Amir Baghbanzadeh, Hamidreza Hassanian, Patrizia Leone, Mahdi Jafarlou, Nazila Alizadeh, Vito Racanelli, and Behzad Baradaran. "The emerging role of noncoding RNAs in systemic lupus erythematosus: new insights into the master regulators of disease pathogenesis." Therapeutic Advances in Chronic Disease 14 (January 2023): 204062232311535. http://dx.doi.org/10.1177/20406223231153572.
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Auto-immune diseases are a form of chronic disorders in which the immune system destroys the body’s cells due to a loss of tolerance to self-antigens. Systemic lupus erythematosus (SLE), identified by the production of autoantibodies in different body parts, is one of the most well-known examples of these diseases. Although the etiology of SLE is unclear, the disease’s progression may be affected by genetic and environmental factors. As studies in twins provide adequate evidence for genetic involvement in the SLE, other phenomena such as metallization, histone modifications, and alterations in the expression of noncoding RNAs (ncRNAs) also indicate the involvement of epigenetic factors in this disease. Among all the epigenetic alterations, ncRNAs appear to have the most crucial contribution to the pathogenesis of SLE. The ncRNAs’ length and size are divided into three main classes: micro RNAs, long noncoding RNAs (LncRNA), and circular RNAs (circRNAs). Accumulating evidence suggests that dysregulations in these ncRNAs contributed to the pathogenesis of SLE. Hence, clarifying the function of these groups of ncRNAs in the pathophysiology of SLE provides a deeper understanding of the disease. It also opens up new opportunities to develop targeted therapies for this disease.
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Gaddam, Maneesh, Olga Alexandra Reyes, Cosmina Zean, and Gilda Diaz-Fuentes. "Still’s disease mimicking sepsis in a young woman. A case report and literature review." Journal of Clinical Case Reports and Studies 1, no. 6 (November 9, 2020): 01–04. http://dx.doi.org/10.31579/2690-8808/022.
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Background Adult onset Still’s disease (ASD) is a rare systemic auto-inflammatory condition that often poses a diagnostic dilemma due to nonspecific clinical signs and symptoms. We report a case of ASD that dramatically improved after a short course of steroids. Case presentation A 23-year-old women from Ghana presented with a two-week history of fever, sore throat, right-sided neck swelling and an evanescent, pruritic rash on her extremities. On exam she was febrile to 103 F, tachycardic, tachypneic, had tender, right-sided cervical lymphadenopathy, and diffuse joint tenderness with decreased range of motion. She was admitted to the ICU for possible sepsis and started on broad-spectrum antibiotics. Extensive work-up for possible infectious and auto-immune etiologies, including a bone marrow biopsy was negative. The diagnosis of Still’s disease was made based on the Yamaguchi criteria. The patient was started on methyl-prednisolone and significantly improved within 24 hours. Conclusion Patients presenting with ASD often represent a diagnostic challenge. Clinicians should be aware of this rare disorder, exclude other more frequent diseases and start early anti-inflammatory therapy to avoid poor outcomes.
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Pandey, Asim, Samriddhi Parajuli, Alok Dhungel, Rahul Devkota, and Angel Dongol. "Etoricoxib Induced Toxic Epidermal Necrolysis in a case of Systemic Lupus Erythematosus: A Case Report." Journal of Nepal Medical Association 60, no. 253 (August 31, 2022): 811–14. http://dx.doi.org/10.31729/jnma.7665.
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Toxic epidermal necrolysis is a potentially life-threatening dermatological condition whose pathogenesis and exact treatment are not yet known. Drugs like anticonvulsants, allopurinol and non-steroidal anti-inflammatory drugs like etoricoxib, a selective cyclo-oxygenase-2 inhibitor prescribed for pain management are associated with a high risk of toxic epidermal necrolysis. It is also associated with immunodeficiency and dysregulated immune reactions like systemic lupus erythematosus, an autoimmune disease in which organs and cells undergo damage initially mediated by tissue binding auto-antibodies and immune complexes. Here, a 34 year old lady was presented in emergency with multiple maculopapular rashes over the neck and trunk region after treatment with etoricoxib for osteoarthritis of the left foot.
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Mohan, Gurinder, Avleen Kaur, and Umang Khullar. "Successful outcome of pregnancy in a case of systemic lupus erythematosus : a case report." International Journal of Advances in Medicine 6, no. 4 (July 24, 2019): 1340. http://dx.doi.org/10.18203/2349-3933.ijam20193138.
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Systemic lupus erythematosus (SLE) is a multisystem, auto immune connective tissue disease that commonly affects women of reproductive age and may coexist with pregnancy. The autoantibodies and immune complexes lead to damage of various organs and tissues. Pregnant woman with SLE have increased risk of spontaneous abortion, preterm delivery, intrauterine growth retardation, preeclampsia, neonatal lupus, stillbirth and intrauterine fetal death. The therapeutic intervention with anticoagulants, steroids, immunosuppressive agents pose a high risk to both mother and fetus. A multidisciplinary approach and close medical, obstetrical and neonatal monitoring leads to optimal outcome. Authors describe a successful management of an antenatal patient with positive antinuclear antibody, anti-ds DNA antibody and antiphospholipid antibody with bad obstetric history. She underwent an emergency cesarean section and delivered a healthy female child.
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Breillat, P., K. Mariampillai, P. Martins, P. Legendre, B. Dunogue, J. L. Charuel, M. Miyara, et al. "POS0323 ANTI PM-SCL ASSOCIATED AUTO IMMUNE DISEASES: MULTICENTRIC COHORT OF 128 PATIENTS." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 388.1–389. http://dx.doi.org/10.1136/annrheumdis-2021-eular.223.
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Background:Autoantibodies permit to classify and subgroup connective tissue diseases (CTD) in homogeneous groups of patients in terms of phenotype and prognosis. Anti PM-Scl antibodies have been associated with different CTD categories such as: idiopathic inflammatory myositis (IIM), systemic sclerosis (SSc), Sjögren’s syndrome (SjS), systemic lupus erythematosus (SLE), mixed connective tissue disease (MCTD) or undifferentiated connective tissue disease (UCTD).Objectives:To determine clinical spectrum of anti-PM-Scl associated disease and if it an homogenous condition.Methods:This multicentric (four hospitals) observational and retrospective study included all consecutive patients with positive testing for anti PM-Scl antibodies on immunoblot assay and connective tissue disease (2011 -2020). Epidemiological, biological, clinical and radiological data were collected in standard form as well as patient’s outcome.Results:One hundred twenty height patients (female n=96;75%) were included. Median [quartiles] age at diagnosis was 50 [18;84] (IQR) and follow-up duration of 7 [3.75-12] years. Seventy-six (59.3%) patients were simple anti-Pm-Scl positive, and 40.7% were associated with other antibodies: anti-SSA/Ro52 (n=13; 10.92%), SSc associated antibodies (n=21; 16.4%), anti-dsDNA for (n=9; 7%), anti-RNP (n=6; 4.7%) and anti-CCP antibodies (n=6; 4.7%). Most patients had cutaneous involvement (n=106; 83%) with skin thickening (n=47; 36%), mechanics hands (n= 28; 22%), calcinosis (n=26; 20.3%) and subcutaneous edema (n=20; 15.62%). Vascular involvement was frequent with Raynaud phenomenon (n= 89; 69%), telangiectasia (n=36; 28%), skin ulcers (n=27; 21%), pulmonary hypertension (n=8/120; 6.7%) and scleroderma renal crisis (n=2; 1.5%). A majority of patients also displayed an interstitial lung disease (ILD) (n=83; 65.8%); nonspecific interstitial pneumonia (92.7%) and/or organizing pneumonia (25.3%). ILD was characterized by a subacute onset in 37/81 (45.7%); median [quartiles] forced vital capacity (FVC) and total lung capacity (TLC) at diagnosis of 88% [73-105] and 79.5% [68.5-101] respectively. Sixty patients (47%) had muscular sign including myalgia (47%), elevated CPK (n=51; 40%) and muscular weakness (Medical Research Council score <4) (n=19/124;15%). Finally, fifty-three (41.7%) had gastroesophageal reflux. Thirty-nine patients (30.4%) experienced at least one muscular or ILD relapse and 6 (4.84%) died during follow-up (2 breast cancer, 1 pneumonia, 3 unknown etiology). Concerning patients’ prognosis, relapses were associated with skeletal (n=29, 74.4% vs n=32, 35.96%, p < 0.001) or cardiac muscle involvement (n=7, 18.4% vs n=2, 2.5%, p=0.007), and subacute ILD (n=19, 65.5% vs n=18, 34.62%, p= 0.05) with organized pneumonia pattern (n=11, 32.3% vs n=10, 13.9%, p=0.05). Strikingly, ILD occurred mainly in men (90.6% vs 57.2%, p < 0.001) and was associated with anti-Scl-70 positivity (n=14, 16.67% vs 0%, p= 0.01). Muscle involvement was associated arthralgia (n=46, 76.67% vs n=34, 50.75%, p=0.005), respiratory signs at diagnosis: dyspnea NYHA ≥3 (n=46, 75.41% vs n=30, 44.78%, p < 0.001), sub-acute ILD (n=24, 61.54% vs n=13, 30.95%, p=0.0111) with lower FVC (73% [64;88] vs 98 [76;105], p < 0.001). Ulcers were associated with Anti-Scl70 positivity (n=9, 33.33% vs n=5, 4.95%, p < 0.001), Raynaud phenomenon (n=27, 100% vs n=62, 61.39%, p < 0.001), digestive involvement (n=20, 74.07% vs n=34, 33.66%, p < 0.001), ILD with chronic onset (n=15, 78.95% vs n=29, 46.77%, p=0.027) and increased incidence of deaths (n=4, 16% vs n=2, 2.02%, p= 0.01).Conclusion:Conducted on the largest cohort of Anti-PM-Scl patients, this study highlights two main phenotypes that determine different outcome and prognosis. One was associated with muscular disease and subacute onset ILD with more frequent relapses. The second with a vascular phenotype associated with chronic ILD, digestive involvement, chronic evolution and increased incidence of death. This could lead to a reclassification of PM-Scl associated auto immune diseases.Disclosure of Interests:None declared
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Zhao, Lin-Pierre, Berenice Schell, Rathana Kim, Marie Sébert, Pierre Lemaire, Maxime Boy, Stéphanie Mathis, et al. "MDS-029: Prevalence of VEXAS Syndrome in MDS/CMML Patients with Systemic Inflammatory and Auto-Immune Disease." Clinical Lymphoma Myeloma and Leukemia 21 (September 2021): S337—S338. http://dx.doi.org/10.1016/s2152-2650(21)01788-2.
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Papadimitriou, Theodoros-Ioannis, Arjan van Caam, Peter M. van der Kraan, and Rogier M. Thurlings. "Therapeutic Options for Systemic Sclerosis: Current and Future Perspectives in Tackling Immune-Mediated Fibrosis." Biomedicines 10, no. 2 (January 29, 2022): 316. http://dx.doi.org/10.3390/biomedicines10020316.
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Systemic sclerosis (SSc) is a severe auto-immune, rheumatic disease, characterized by excessive fibrosis of the skin and visceral organs. SSc is accompanied by high morbidity and mortality rates, and unfortunately, few disease-modifying therapies are currently available. Inflammation, vasculopathy, and fibrosis are the key hallmarks of SSc pathology. In this narrative review, we examine the relationship between inflammation and fibrosis and provide an overview of the efficacy of current and novel treatment options in diminishing SSc-related fibrosis based on selected clinical trials. To do this, we first discuss inflammatory pathways of both the innate and acquired immune systems that are associated with SSc pathophysiology. Secondly, we review evidence supporting the use of first-line therapies in SSc patients. In addition, T cell-, B cell-, and cytokine-specific treatments that have been utilized in SSc are explored. Finally, the potential effectiveness of tyrosine kinase inhibitors and other novel therapeutic approaches in reducing fibrosis is highlighted.
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Kini, Sandesh, Ramesh Bhat Y, Chennakeshava Thunga, Sowmya Shashidhara, and Akshatha Anand. "Clinical and Immunological Spectrum of Systemic Lupus Erythematosus in Children." Journal of Nepal Paediatric Society 40, no. 1 (August 10, 2020): 14–20. http://dx.doi.org/10.3126/jnps.v40i1.28460.
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Introduction: Systemic Lupus Erythematosus (SLE) is an auto immune disorder affecting mainly adolescent females and young women of reproductive age. The disease is characterised by widespread inflammation of blood vessels and connective tissues due to the presence of anti-nuclear antibodies (ANA). There are limited number of studies from South India on paediatric lupus. Our objectives were to study the clinical and immunological features of childhood SLE along with treatment modalities and its outcome at the end of one year follow up. The correlation between various auto-antibodies and systemic involvement was also assessed.
Methods: This was a retrospective observational study carried out in paediatric unit at a tertiary care centre in South India. Data was obtained through patient’s medical records. From April 2003 to April 2019, 32 children were diagnosed to have SLE as per the American college of Rheumatology 1997 criteria.
Results: The study population included 32 children fulfilling the criteria. Female to male ratio was 4.3:1. The mean age at diagnosis was 11.52 years. The most common clinical manifestations were renal (87.5%) followed by haematological (81.3%), musculoskeletal (59.4%), mucocutaneous (53.1%) and nervous system (31.3%) involvement. All patients were positive for anti-nuclear antibodies. Anti-double stranded DNA (78.1%) was the most common auto-antibody profile followed by anti-ribosomal p protein (37.5%) and anti-nucleosome antibody (37.5%). During the follow up, 13 (40.6%) children attained complete remission, 10 (31.2%) went into partial remission and nine (28.1%) had persisting active disease.
Conclusion: The clinical spectrum and outcome of paediatric SLE depends upon the age of presentation and number of organ systems involved at the time of diagnosis. Our study throws light on various aspects of SLE in children from developing countries like India.
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Sudhakar, P., B. Verstockt, J. Cremer, S. Verstockt, J. Sabino, M. Ferrante, and S. Vermeire. "DOP08 Transcriptional signatures of blood derived immune cells associated with disease location-based heterogeneity in IBD." Journal of Crohn's and Colitis 16, Supplement_1 (January 1, 2022): i058. http://dx.doi.org/10.1093/ecco-jcc/jjab232.047.
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Abstract Background Disease location is a prominent axis of heterogeneity in Inflammatory Bowel Disease (IBD) with many implications. Using genome-wide profiling of the transcriptome of monocytes and CD4+ T cells isolated and purified from whole blood, we aimed to identify molecular signatures and mechanisms associated with different locations among IBD patients. Methods Blood was collected from 125 IBD patients (87 CD, 38 UC) with endoscopy-proven active disease (presence of ulcerations). Cell separation and fluorescence activated cell sorting were performed to separate the monocyte and CD4+ T cell fractions, from which RNA was subsequently isolated and sequenced (Illumina HiSeq 4000NGS). We used different supervised and unsupervised approaches (differential expression, pathway based data integration, latent factor based models, regularized generalized canonical correlation analysis and co-expression networks) to interpret the differences in the gene expression datasets of monocytes and CD4+ T cells from patients with different disease locations (Montreal classification). Functional enrichment analysis was performed using the ReactomePA package. Regulatory relationships and therapeutic relevance information were retrieved from the ChEA3 and the OpenTargets resources respectively. Comparison with single-cell and bulk-derived gene expression signatures from other auto-immune diseases were performed using the ADEX resource. Results Highly variant disease-location (DL)-associated genes (FDR <= 0.1) in monocytes and CD4+ T cells were identified using latent factor based unsupervised models. These genes were known to be involved in IBD pathogenesis and/or intestinal inflammation. Additional supervised analysis revealed significant differences in CD4+ T cells between ileal CD patients and UC patients. RAF-independent MAPK-activation pathway and FOXO-mediated transcriptional pathway (downregulated in UC patients) were over-represented (FDR <= 0.05) among the features distinguishing ileal CD and UC patients based on signature sets derived from the above-mentioned multiple approaches. Of note was the finding that 12.5% of the DL associated co-expression modules were also annotated as IBD drug targets. Based on gene expression signature from bulk and single-cell sources, the DL associated genes were found to be active in many other auto-immune diseases such as rheumatoid arthritis, systemic sclerosis, Sjögren’s syndrome, type 1 diabetes and Systemic lupus erythematosus, suggesting their role in mediating immune malfunctions. Conclusion We identified signaling pathways and transcription factors which could drive the expression differences observed in the circulating immune cells between ileal CD and UC patients.
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Aguilera-Galaviz, Luis, Martha Hernandez-Montoya, Maria Lopez Luna, Iris Garcia, and Maria Aceves-Medina. "Hsp90 and autoantibodies expression in periodontal disease (120.29)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 120.29. http://dx.doi.org/10.4049/jimmunol.188.supp.120.29.
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Abstract In Periodontal disease (PD)several studies suggest, that exaggerated host immune and inflammatory response is considered as a potential risk for developing cardiovascular diseases, alter the course of diabetes, osteoporosis and premature babies during pregnancy. Objetives: the baseline of this study was to detect the presence of auto-antibodies and Hsp90 expression in healthy and systemic compromised patient. Methods: 32 patients with periodontitis were evaluated and 20 healthy people, blood sample to set up IFI for ANCA, antiepithelial antibodies, ANA and WB to determine the molecular profile using keratinocyte extract RT-PCR for Hsp 90 was performed in periodontal tissue. Results: 57% were positives for ANCA, the total of sera were positives for nuclear and/or cytoplasmic antibodies and 57% presented anti-epithelial antibodies, the sera from these patients recognized proteins in a wide range of molecular weight keratinocytes extract, and 30 and 70 kD in mouse skin extract, Hsp90 expression was considerably highest in PD patient and systemic compromise. Conclusions: The immune response in periodontal disease is influenced by the microflora, the production of antibodies against self structures, could be involved in the pathogenic mechanism; these autoantibodies are associated with necrotic or apoptotic phenomena. Metabolic activity of microorganism should be involved in cross reactions and antigen procesesing in situ could stimulate self reactive lymphocytes.
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Morales, Jessica, Yerania Rodriguez, Karina Vila, Martha Ricaurte, Luis M. Vila, and Anthony V. Washington. "TLT-1 as a possible modulator of Systemic Lupus Erythematosus." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 210.10. http://dx.doi.org/10.4049/jimmunol.198.supp.210.10.
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Abstract Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by immune system hyperactivity and autoantibody production that can affect almost any organ system. TREM like transcript-1 (TLT-1) is a membrane receptor found in platelet α-granules with a soluble form (sTLT-1) detected in serum but not plasma of healthy individuals. The evaluations of patients suffering from diseases, such as sepsis, show a significant increase of plasma sTLT-1 levels. It is not known if TLT-1 plays a role in auto immune diseases such as Lupus. In the present study we evaluate the potential that TLT-1 may play a role in the etiology of SLE. We assessed the plasma of 46 SLE patients and compared to 28 healthy controls by ELISA. Our results showed that SLE patients had a significant decrease in plasma sTLT-1 levels compared to healthy controls (9.0 [7.2] vs. 18.6 [22.3] ng/ml, p=0.008). A negative correlation was observed between TLT-1 levels and LupusPRO [lupus symptoms (r = −0.388, p = 0.055). Based on this data; we hypothesized that SLE patients produce autoantibodies against TLT-1 in serum which might correlate with clinical aspects of the disease. To address this question; TLT-1 antibodies levels in serum were measured by ELISA. Our data suggests that a sub-population of SLE patients have TLT-1 autoantibodies. This data was further confirmed by confocal microscopy. Using HEK cells stably transfected with TLT-1; we evaluated the serum of SLE patients for the presence of TLT-1 autoantibodies using immunofluorescence. Our data confirms that a sub-population of SLE patients with active disease expresses antibodies against TLT-1 suggesting a possible role for TLT-1 during the pathogenesis of SLE and targets new treatment possibilities for lupus patients.
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Audia, Sylvain, Natacha Grienay, Morgane Mounier, Marc Michel, and Bernard Bonnotte. "Evans’ Syndrome: From Diagnosis to Treatment." Journal of Clinical Medicine 9, no. 12 (November 27, 2020): 3851. http://dx.doi.org/10.3390/jcm9123851.
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Evans’ syndrome (ES) is defined as the concomitant or sequential association of warm auto-immune haemolytic anaemia (AIHA) with immune thrombocytopenia (ITP), and less frequently autoimmune neutropenia. ES is a rare situation that represents up to 7% of AIHA and around 2% of ITP. When AIHA and ITP occurred concomitantly, the diagnosis procedure must rule out differential diagnoses such as thrombotic microangiopathies, anaemia due to bleedings complicating ITP, vitamin deficiencies, myelodysplastic syndromes, paroxysmal nocturnal haemoglobinuria, or specific conditions like HELLP when occurring during pregnancy. As for isolated auto-immune cytopenia (AIC), the determination of the primary or secondary nature of ES is important. Indeed, the association of ES with other diseases such as haematological malignancies, systemic lupus erythematosus, infections, or primary immune deficiencies can interfere with its management or alter its prognosis. Due to the rarity of the disease, the treatment of ES is mostly extrapolated from what is recommended for isolated AIC and mostly relies on corticosteroids, rituximab, splenectomy, and supportive therapies. The place for thrombopoietin receptor agonists, erythropoietin, immunosuppressants, haematopoietic cell transplantation, and thromboprophylaxis is also discussed in this review. Despite continuous progress in the management of AIC and a gradual increase in ES survival, the mortality due to ES remains higher than the ones of isolated AIC, supporting the need for an improvement in ES management.
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Yap, Desmond Yat Hin, and Kar Neng Lai. "Cytokines and Their Roles in the Pathogenesis of Systemic Lupus Erythematosus: From Basics to Recent Advances." Journal of Biomedicine and Biotechnology 2010 (2010): 1–10. http://dx.doi.org/10.1155/2010/365083.
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Systemic lupus erythematosus (SLE) is a complex auto-immune disorder which involves various facets of the immune system. In addition to autoantibody production and immune complex deposition, emerging evidences suggest that cytokines may act as key players in the immunopathogenesis of SLE. These cytokines assume a critical role in the differentiation, maturation and activation of cells and also participate in the local inflammatory processes that mediate tissue insults in SLE. Certain cytokines such as the IL-6, IL-10, IL-17, BLys, type I interferons (IFN) and tumor necrosis factor-α(TNF-α) are closely linked to pathogenesis of SLE. The delineation of the role played by these cytokines not only fosters our understanding of this disease but also provides a sound rationale for various therapeutic approaches. In this context, this review focuses on selected cytokines which exert significant effect in the pathogenesis of SLE and their possible clinical applications.
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Singh, Aditi. "Systemic lupus erythematosus masquerading as gangrene − an infrequent presentation." Egyptian Journal of Dermatology and Venereology 43, no. 3 (August 25, 2023): 220–21. http://dx.doi.org/10.4103/ejdv.ejdv_42_22.
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Systemic lupus erythematosus (SLE) is an auto-immune disease affecting multiple organs. Among the cutaneous features, digital gangrene is considered to be very rare, occurring in only 1.3% of SLE patients. It is considered to be due to compromised perfusion of digits secondary to vasculitis, vasospasm and thomboembolism. This is the case report of a 35-year-old female who presented with acute blackish discoloration of toes of both feet associated with pain. She had no other features of SLE. But serology came out positive for SLE. The patient responded well to steroids, hydroxychloroquine, antiplatelet and anticoagulant medications and is currently under follow-up. This case report basically shows us that SLE should be considered as a possible differential diagnosis whenever there is a young patient presenting with digital gangrene without any other medical history.
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Doglio, Matteo, Alessia Ugolini, Clara Bercher, Cristiano Toma, Chiara Bonini, Fabio Ciceri, Barbara Camisa, et al. "CAR-T Cells for Systemic Lupus Erythematosus." Blood 142, Supplement 1 (November 28, 2023): 6813. http://dx.doi.org/10.1182/blood-2023-189673.
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Systemic Lupus Erythematosus (SLE) is an autoimmune disease characterized by an abnormal inflammatory response against nuclear antigens with consequent tissue damage. Autoreactive B cells and auto-antibodies have a fundamental role in SLE pathogenesis. Lupus nephritis (LN) has a great impact on patients' survival and quality of life and still represents and unmet clinical need due to the lack of specific treatments and to the poor response to conventional immunosuppression. Regulatory T cells (Tregs) physiologically maintain the immune tolerance and are impaired in SLE. Polyclonal Treg transfer obtained unsatisfactory results due to the low number of disease-relevant antigen-specific cells. Chimeric Antigen Receptors (CARs) are molecules capable of redirecting T cell specificity. CAR-Tregs proved effective in pre-clinical mouse models of autoimmunity. We aimed at developing a CAR-Treg based product to be employed in SLE in particular in LN. We isolated Tregs from Healthy Donors Peripheral Blood Mononuclear Cells (PBMCs) and expanded them with IL-2 and rapamycin. We transduced Tregs with a Lentiviral Vector encoding for a second-generation anti-CD19 CAR, considering the relevant role of autoreactive B cells and autoantibodies in SLE. Engineered cells retained their immune suppressive capabilities upon polyclonal stimulation. Noticeably, they acquired new antigen-specific suppressive capacities, being able to block autologous B cell proliferation. We set up a humanized mouse model of SLE. In vivo, CAR-Tregs delayed the occurrence of B cell lymphopenia, producing immunomodulatory cytokines and without showing toxicity or reprogramming towards Th17 pro-inflammatory cells. In inflamed organs, CAR-Tregs restored the normal composition of the immune system. In conclusion, we efficiently generated anti-CD19 CAR-Tregs and proved their efficacy both in vitro and in an in vivo humanized mouse model of lupus.
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Anjana Sujith, Lohith B A, Muralidhar P. Pujar, and Ashvini Kumar M. "Ayurvedic approach in the functional improvement of Systemic Lupus Erythematosus (SLE) - A Case Report." Journal of Ayurveda and Integrated Medical Sciences 8, no. 12 (February 1, 2024): 265–68. http://dx.doi.org/10.21760/jaims.8.12.40.
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Systemic lupus erythematosus (SLE) is an auto immune disease in which organs and cells undergo damage mediated by tissue-binding autoantibodies and immune complex.[1]. 90% of patients are women of child-bearing years are affected with this disease. According to Ayurveda, the signs and symptoms can be included under the purview of Vataraktha. Case summary: A 43-year-old female patient approached with chief complaints of pain over bilateral elbow joints, shoulder joints and low back pain, burning sensation over toes for 8 years associated with febrile attacks, coated tongue, mouth ulcer, dryness of mouth aggravated since 2 months. The Ayurvedic diagnosis was made as Vataraktha on the basis of signs and symptoms. The patient was given Sadyovirechana (Purgation therapy), Basti therapy (enema) along with other external procedures and internal medications. Significant improvement was observed after the treatment in terms of VAS Score and other subjective parameters. This case study shows that Ayurvedic treatment is helpful in the functional improvement of SLE and helps in improving the quality of life.
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A. Ali, Fattma. "Impact the Connection Between Adaptive Immunity and Systemic Lupus Erythematous." Journal of Clinical Surgery and Research 6, no. 1 (January 28, 2025): 01–08. https://doi.org/10.31579/2768-2757/155.
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Background: Systemic lupus erythematosus (SLE) is a systemic autoimmune disorder of unknown etiology that mostly impact females. SLE illness is defined by the emergence of auto antibodies and the accumulation of immune complexes, leading to inflammation and tissue damage in multiple organs. Patients suffering from this condition may display pathological harm to several organs such as the kidneys, skin, joints, blood, or neurological system. Objectives: Our study aimed to carry out the role of the adaptive immunity including the main cells of adaptive immunity T cells, B cells, IL-6, IL-10 in the systemic lupus erythematous autoimmune disease. Main body: T lymphocytes immune tolerance. The breakdown is a crucial factor in the development of SLE and T lymphocytes perform a significant role in this pathway. It may result in triggering and stimulation of B lymphocytes and dendritic cells at sites of inflammation, as well as abnormal release of cytokines and cellular signaling. B lymphocytes in patients with SLE suffer from impaired regional and peripheral tolerance. Lupus arises from an abundance of self-reactive B lymphocytes that produce a variety of auto antibodies. Interactions between T cells and B cells are widely recognized. IL-6, a type of inflammatory cytokine, has been linked to the development of SLE in both mice and humans based on scientific research. IL-10 has been observed to have two distinct functions in SLE patients. It is a cytokine that reduces inflammation by preventing the production of other cytokines that promote inflammation, such as IFN-c. In addition, IL-10 plays a role in the B cell function, resulting in the growth and specialization of B cells, the switching of antibody classes, and the reduction of B cell mortality in germinal centers, so facilitating the creation of autoantibodies. Conclusion: The underlying mechanisms of SLE are not yet understood completely. Multiple predisposing factors are likely involved in the development of SLE and play a crucial role in triggering and sustaining aberrant immunological reactions. Nevertheless, the precise mechanism by which the disease develops is still not fully understood.
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Zhao, Lin-Pierre, Berenice Schell, Rathana Kim, Marie Sébert, Pierre Lemaire, Maxime Boy, Stéphanie Mathis, et al. "Poster: MDS-029: Prevalence of VEXAS Syndrome in MDS/CMML Patients with Systemic Inflammatory and Auto-Immune Disease." Clinical Lymphoma Myeloma and Leukemia 21 (September 2021): S229. http://dx.doi.org/10.1016/s2152-2650(21)01444-0.
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Satav, Durga Gorakh. "SYSTEMIC LUPUS ERYTHEMATOUS (SLE) and RHEUMATOID ARTHRITIS WITH AYURVEDIC INTERPRETATION." SCHOLARLY RESEARCH JOURNAL FOR INTERDISCIPLINARY STUDIES 9, no. 68 (October 31, 2021): 16299–305. http://dx.doi.org/10.21922/srjis.v9i68.10027.
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Autoimmune diseases are pathological conditions identified by abnormal autoimmune responses and characterised by auto antibodies and T cell responses for self molecules by immune system reactivity. Autoimmune disorders include rheumatoid arthritis, systemic lupus erythematosu (SLE), Crohn’s disease, Graves’ disease, Hashimoto’s thyroiditis, Insulin dependent diabetes mellitus, Multiple sclerosis, Myasthenia Gravis, Psoriasis , Inflammatory bowel disease (IBD) and vasculitis. Human autoimmune diseases affecting in aggregate more than the 5% of the population worldwide. Aim Interpretation of SLE with pittanubandhi Amavata and Rheumatoid Arthritis (Amavata) with vata kapha anubandhi amavata. Objectives 1. To study the sign and symptoms of SLE and Rheumatoid arthritis. 2. To study the sign and symptoms of Rheumatoid arthritis with reference to pittanubandhi Amavata. 3. To study the common sign and symptoms of both SLE and pittanubandhi Amavata. Material and Methods This review article is based on various references of SLE, rheumatoid arthritis and classical references of Amavata are collected. Conclusion SLE is the classical example of systemic autoimmune disease. It most often harms the heart, joints, lungs and skin, blood vessels, kidneys and nervous system. In Ayurveda, symptoms of vata kapha anubandhi amavata in Ayurveda closely resembles with rheumatoid arthritis and symptoms of pitta anubandhi amavata can be correlated with SLE as there is a great involvement of pitta dosha and rakta dhatu in SLE. And pitta dosha lies within Rakta dhatu in body. i.e. Ashrayashrayi sambandha. Preventive measures are like Langhana, Deepana-Pachana, Shodhana, Shaman and Rasayan have been described for the management of Amvata are actually more effective.
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Zhang, Chen, Shijie Cai, Ying Li, Xiaoyan Xu, Yonghui Liu, Huaiyu Qiao, Chun-Kwok Wong, Guoqiu Wu, Hui Jin, and Xun Gao. "Elevation of Metrnβ and Its Association with Disease Activity in Systemic Lupus Erythematosus." International Journal of Molecular Sciences 24, no. 17 (September 2, 2023): 13607. http://dx.doi.org/10.3390/ijms241713607.
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Systemic lupus erythematosus (SLE) is an auto-immune disease, the pathogenesis of which remains to be fully addressed. Metrnβ is a novel cytokine involved in the pathogenesis of inflammatory disease, but its regulatory roles in SLE are unclear. We aimed to comprehensively investigate the clinical value of Metrnβ in SLE. A massive elevation of circulating Metrnβ levels was observed in SLE, and patients with an active phase displayed higher Metrnβ concentrations than those with inactive phases. Additionally, we found that Metrnβ expression was positively correlated with clinical indicators of SLE. Longitudinal cytokine and chemokine profiles revealed a disturbed immune response in SLE, with high activity profiles displayed severe pathogenic inflammation, and a positive correlation of the serum Metrnβ with CXCL9, IL10, IL18 and IL1RA was observed as well. Moreover, Metrnβ expressions exhibited an inverse correlation with Treg and B10. Of note, a significant decrease of ILC2 was found in SLE, and there was a negative correlation of Metrnβ with ILC2 as well. Further ROC analysis showed that the area under the curve (AUC) for Metrnβ was 0.8250 (95% CI: 0.7379–0.9121), with a cutoff value of 1131 pg/mL to effectively distinguish SLE patients from healthy controls. Our study herein demonstrated for the first time that Metrnβ values were increased and were immunologically correlated with SLE activity, which could be utilized as an alternative biomarker for the early identification and predicting of the immuno-response of SLE.
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Ling, Leona E., Sucharita Roy, Thomas Daly, Edward Cochran, Steven Tyler, Lynn Markowitz, Dorota Bulik, et al. "M281: A Therapeutic Anti-FcRn Blocking Antibody for Rapid Clearance of IgG and IgG Autoantibodies in Immune Cytopenias and Other Auto/Allo-Immune Disease." Blood 126, no. 23 (December 3, 2015): 3472. http://dx.doi.org/10.1182/blood.v126.23.3472.3472.
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Abstract Introduction IgG antibodies are the primary pathogenic agent in a number of auto- or allo-immune diseases. Efficacious therapies which decrease systemic levels of pathogenic antibodies include treatment with IVIG therapeutic plasmapheresis or immunoabsorption. Here, a novel strategy was evaluated to induce IgG clearance in diseases driven by IgG autoantibodies by blockade of FcRn-mediated IgG recycling. Methods M281 was developed as a high affinity, effectorless IgG1anti-FcRn monoclonal antibody. M281 effect on IgG recycling was evaluated in human umbilical vein endothelial cells in vitro. In vivo studies in transgenic human FCGRT/mouse FCGRT null mice and cynomolgus monkey were performed to characterize the pharmacokinetics, biodistribution, target occupancy, specificity of M281 and its efficacy in mouse models of thrombocytopenia and arthritis. Results M281 demonstrates specific dose-dependent, albumin-sparing IgG clearance in human FCGRT transgenic/mouse FCGRT null mice and in cynomolgus monkeys. M281 inhibits IgG recycling in endothelial cells in vitro and IgG clearance in vivo. Pharmacokinetics, target occupancy, pharmacodynamics and biodistribution indicate typical recombinant antibody biodistribution with rapid, dose dependent target inhibition and systemic clearance. M281 also demonstrated efficacy in mouse idiopathic thrombocytopenia purpura and collagen antibody-induced arthritis models of disease. Conclusions These findings support the evaluation of M281 as a strategy for the rapid and reversible suppression of pathogenic autoantibodies or alloantibodies in the setting of immune cytopenias, acquired inhibitors, thrombotic states and other disorders. Disclosures Ling: Momenta Pharmaceuticals: Employment, Equity Ownership. Roy:Momenta Pharmaceuticals: Employment, Equity Ownership. Daly:Momenta Pharmaceuticals: Employment, Equity Ownership. Cochran:Momenta Pharmaceuticals: Employment, Equity Ownership. Tyler:Momenta Pharmaceuticals: Employment, Equity Ownership. Markowitz:Momenta Pharmaceuticals: Employment, Equity Ownership. Bulik:Momenta Pharmaceuticals: Employment, Equity Ownership. Choudhury:Momenta Pharmaceuticals: Employment, Equity Ownership. Meador:Momenta Pharmaceuticals: Employment, Equity Ownership. Parge:Momenta Pharmaceuticals: Employment. Mekala:Momenta Pharmaceuticals: Employment, Equity Ownership. Sipsey:Momenta Pharmaceuticals: Employment, Equity Ownership. Gurnani:Momenta Pharmaceuticals: Employment, Equity Ownership. Duffner:Momenta Pharmaceuticals: Employment, Equity Ownership. Lee:Momenta Pharmaceuticals: Employment, Equity Ownership. Washburn:Momenta Pharmaceuticals: Employment, Equity Ownership. Meccariello:Momenta Pharmaceuticals: Employment, Equity Ownership. Schaeck:Momenta Pharmaceuticals: Employment, Equity Ownership. Wang:Momenta Pharmaceuticals: Employment, Equity Ownership. Schultes:Momenta Pharmaceuticals: Employment, Equity Ownership. Hillson:Momenta Pharmaceuticals: Employment, Equity Ownership. Avery:Momenta Pharmaceuticals: Employment, Equity Ownership. Kaundinya:Momenta Pharmaceuticals: Employment, Equity Ownership. Manning:Momenta Pharmaceuticals: Employment, Equity Ownership.
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Dinu, Irina, Mihai Abobului, Claudia-Oana Cobilinschi, Ioana Saulescu, Andra Balanescu, and Daniela Opris-Belinski. "COVID-19, a phantomatic trigger for relapsing polychondritis." Romanian Journal of Rheumatology 31, no. 3 (September 30, 2022): 124–27. http://dx.doi.org/10.37897/rjr.2022.3.4.
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Relapsing polychondritis (RP) is an auto-immune disease which affects the cartilaginous parts of sites like the ear, nose or upper respiratory tract. The condition can also involve other cartilage-containing structures such as the eyes, joints, the heart, kidneys and central nervous system. Early diagnosis of RPis essential for preventing significant damage to vital organs that can lead to increased morbi-mortality rates. First-line therapy in RP is systemic glucocorticoids, while in refractory cases monoclonal antibodies can be used despite scarcity of efficacy data available in published literature. The link between RP and neoplasia, especially hematological malignancy, should not be omitted when screening patients with suspicion of RP diagnosis. The onset of COVID-19 pandemic has generated a new source of immune mediated pathologies, such as small vessel vasculitis, immune thrombocytopenic purpura or Guillain-Barre syndrome and other auto-inflammatory syndromes triggered by COVID-19 seem to unveil. The present case depicts a female patient who presented with erythematous and painful areas of her right ear after priorly experiencing similar episodes in both ears and nose bridge shortly after having the COVID-19 vaccine booster dose.
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Khan, Sana, Arghadip Das, Khalid Mahmood Uddin, Shamail Zia, Areij Khan, Marrium S. Memon, Danial Hassan, Sharmeen Naz, and Sarah Khalid. "Psoriasis and its Variants." National Journal of Health Sciences 7, no. 4 (December 30, 2022): 181–92. http://dx.doi.org/10.21089/njhs.74.0181.
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Abstract: Background: Psoriasis is a chronic, immune-mediated, inflammatory illness of the skin which is quite common. The typical lesions are well demarcated, flaky and erythematous plaques that are frequently observed on the extensor regions. Psoriasis causes vasodilatation and hyper proliferation of keratinocytes expressed as thickened and erythematous skin, generally covered with silver gray scales. Although the etiology of this disease is not very clear, yet there may be genetic and environmental implications. There are a number of variants of psoriasis which include palm plantar, pustular, erythrodermic, and guttate types. Psoriasis is related to several systemic impediments and coexisting illnesses rendering a great effect on patients. Psoriasis displays coexistence of both autoimmune and auto inflammatory reactions and the stability between the two is important for clinical and histopathological demonstration. Chronic plaque psoriasis shows adaptive immune responses whereas pustular psoriasis displays innate a auto inflammatory responses. Histopathological analysis is the main diagnostic tool for atypical and controversial situations which aids in discerning psoriasis from other dermatoses; biopsy is seldom required for typical psoriasis.
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Faiez, Amouri. "Role of S protein in thromboembolic complications during COVID19 and activated protein C as a serious therapeutic avenue in severe forms of patients." Journal of Applied and Natural Science 12, no. 2 (May 9, 2020): 88–90. http://dx.doi.org/10.31018/jans.vi.2251.
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COVID-19 (Coronavirus disease 2019) is a public health emergency of international concern. There is a pressing urgency to find treatments based upon currently available scientific knowledge and epidemiological data. In this article, we provide a novel hypothesis describing how the severity of the pathology is mainly resulting from the Antibody responses to SARS-CoV-2 (virus causing COVID-19) and not due to the direct action of the virus. SARS-CoV-2 appears to alter the endothelial cell. The pathophysiological mechanism is not yet elucidated. The damage caused resembles a systemic, multi-organ vasculitis predominantly in the lungs. An increase in thromboembolic complications has been observed in COVID-19 patients. These are manifested by pulmonary embolisms or systemic microembolism manifested by microangiopathy affecting the lungs, brain, liver, kidneys and intestines. Therefore, we hypothesize that an auto-immune acquired Protein S (PS) deficiency may be involved in the pathogenesis of thrombotic events in Covid-19. Auto-antibodies to Protein S may form immune complexes, inducing increased clearance of PS or interfering with the protein C-protein S system. COVID-19 early thromboprophylaxis in infected patients, or even effective anticoagulation, could prevent the progression to severe forms, thus reducing mortality in patients with COVID-19. Activated Protein C (APC), a physiological coagulation inhibitor with cytoprotective properties, could be an interesting avenue for the treatment of severe forms of the disease in intensive care; its administration in hypoxic patients could improve tissue oxygenation. Randomized resuscitation studies in patients with COVID19 are also needed to confirm our hypothesis.
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Garzon, Hernan Santiago, and Lina Suarez. "Periodontal disease: from infection to autoimmunity." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 178.4. http://dx.doi.org/10.4049/jimmunol.202.supp.178.4.
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Abstract Five decades of publications have been necessary to document the relationship between immune response and tissue injury in periodontitis. Multiple mechanisms have been implicated in the progression of tissue damage, including the controversial mechanisms of autoimmunity. The aim of this paper is the development of the theories that considered periodontal disease as an autoimmune entity with a historical narrative and descriptive view. Diverse theories have been referenced involving the innate and acquired immunity: generation of anti-neutrophil cytoplasmic antibodies (ANCA), Th17 cell function and IL-17, auto-antibodies to collagen and epithelial components of the periodontium, the role of NK cells T lymphocytes and T CD5, development of molecular mimicry, among others. In conclusion, it’s still difficult to classify periodontal disease as an stabilshed autoimmune disease, because its multifactorial nature makes it difficult to understand. However, the evidence is clear and comprehensive showing related autoimmune mechanisms, which could eventually explain the progression and its relation to systemic events such as cardiovascular disease and atherosclerosis.