Artículos de revistas: "Immune response Molecular aspects"

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AS, Dr Maniyammai, Dr Amudha M, Dr Renuka Devi R, Dr Esther Nalini H, and Dr Arun Kumar Prasad. "Adaptive immune response: Molecular aspects of periodontal disease." International Journal of Applied Dental Sciences 7, no. 4 (October 1, 2021): 89–92. http://dx.doi.org/10.22271/oral.2021.v7.i4b.1356.

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Goodman, Jesse L. "Molecular Aspects of Immune Response in Infectious Diseases." Clinical Infectious Diseases 13, no. 3 (May 1, 1991): 530. http://dx.doi.org/10.1093/clinids/13.3.530-a.

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3

Inman, R. D. "Immunogenetic aspects of host immune response." Canadian Journal of Microbiology 34, no. 3 (March 1, 1988): 319–22. http://dx.doi.org/10.1139/m88-058.

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The central role of histocompatibility leukocyte antigens (HLA) class II molecules in antigen presentation has received great attention in recent years, yet class I molecules have been defined as primarily functioning as a restriction element for cytotoxic T cell killing of virus-infected cells. Extensive clinical evidence, however, indicates that the HLA class I genes are strongly associated with nonseptic complications of enteric and genitourinary bacterial infections. Ninety percent of patients with Reiter's syndrome and reactive arthritis are positive for HLA-B27, yet the mechanism of disease susceptibility conferred by this gene remains obscure. Hypotheses concerning this interaction include (i) class I antigens functioning as receptors for microbial antigens; (ii) class I antigens expressing determinants that cross-react with microbial antigens; and (iii) class I genes controlling immunoregulatory functions that dictate qualitative differences in immune response to pathogenic organisms. These hypotheses await formal testing and hold great promise for understanding immunogenetic control of immune responses in general.

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4

Jeffries, Donald. "Book Review: Molecular Aspects of Immune Response and Infectious Diseases." International Journal of STD & AIDS 2, no. 3 (May 1991): 218. http://dx.doi.org/10.1177/095646249100200322.

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Stetson, C. A., and E. Jensen. "HUMORAL ASPECTS OF THE IMMUNE RESPONSE TO HOMOGRAFTS *." Annals of the New York Academy of Sciences 87, no. 1 (December 15, 2006): 249–57. http://dx.doi.org/10.1111/j.1749-6632.1960.tb23198.x.

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INNES, ELISABETH A., DAVID BUXTON, STEPHEN MALEY, STEPHEN WRIGHT, JOANNE MARKS, IRMA ESTEBAN, ALISTAIR RAE, ALEX SCHOCK, and JONATHAN WASTLING. "Neosporosis: Aspects of Epidemiology and Host Immune Response." Annals of the New York Academy of Sciences 916, no. 1 (January 25, 2006): 93–101. http://dx.doi.org/10.1111/j.1749-6632.2000.tb05278.x.

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Sonenshine, Daniel, E. "Molecular characterization and related aspects of the innate immune response in ticks." Frontiers in Bioscience Volume, no. 13 (2008): 7046. http://dx.doi.org/10.2741/3209.

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Nikolic, Dejan, Milena Jankovic, Bojana Petrovic, and Ivana Novakovic. "Genetic Aspects of Inflammation and Immune Response in Stroke." International Journal of Molecular Sciences 21, no. 19 (October 8, 2020): 7409. http://dx.doi.org/10.3390/ijms21197409.

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Genetic determinants play important role in the complex processes of inflammation and immune response in stroke and could be studied in different ways. Inflammation and immunomodulation are associated with repair processes in ischemic stroke, and together with the concept of preconditioning are promising modes of stroke treatment. One of the important aspects to be considered in the recovery of patients after the stroke is a genetic predisposition, which has been studied extensively. Polymorphisms in a number of candidate genes, such as IL-6, BDNF, COX2, CYPC19, and GPIIIa could be associated with stroke outcome and recovery. Recent GWAS studies pointed to the variant in genesPATJ and LOC as new genetic markers of long term outcome. Epigenetic regulation of immune response in stroke is also important, with mechanisms of histone modifications, DNA methylation, and activity of non-coding RNAs. These complex processes are changing from acute phase over the repair to establishing homeostasis or to provoke exaggerated reaction and death. Pharmacogenetics and pharmacogenomics of stroke cures might also be evaluated in the context of immuno-inflammation and brain plasticity. Potential novel genetic treatment modalities are challenged but still in the early phase of the investigation.

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Petean, Igor Bassi Ferreira, Alice Corrêa Silva-Sousa, Tamara Justiniano Cronenbold, Jardel Francisco Mazzi-Chaves, Lea Assed Bezerra da Silva, Raquel Assed Bezerra Segato, Guilherme Assed Piedade de Castro, Erika Calvano Kuchler, Francisco Wanderley Garcia Paula-Silva, and Manoel Damião Sousa-Neto. "Genetic, Cellular and Molecular Aspects involved in Apical Periodontitis." Brazilian Dental Journal 33, no. 4 (August 2022): 1–11. http://dx.doi.org/10.1590/0103-6440202205113.

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Abstract The development, establishment and repair of apical periodontitis (AP) is dependent of several factors, which include host susceptibility, microbial infection, immune response, quality of root canal treatment and organism's ability to repair. The understanding of genetic contributions to the risk of developing AP and presenting persistent AP has been extensively explored in modern Endodontics. Thus, this article aims to provide a review of the literature regarding the biochemical mediators involved in immune response signaling, osteoclastogenesis and bone neoformation, as the genetic components involved in the development and repair of AP. A narrative review of the literature was performed through a PUBMED/MEDLINE search and a hand search of the major AP textbooks. The knowledge regarding the cells, receptors and molecules involved in the host's immune-inflammatory response during the progression of AP added to the knowledge of bone biology allows the identification of factors inherent to the host that can interfere both in the progression and in the repair of these lesions. The main outcomes of studies evaluated in the review that investigated the correlation between genetic polymorphisms and AP in the last five years, demonstrate that genetic factors of the individual are involved in the success of root canal treatment. The discussion of this review gives subsides that may help to glimpse the development of new therapies based on the identification of therapeutic targets and the development of materials and techniques aimed at acting at the molecular level for clinical, radiographic and histological success of root canal treatment.

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McNamara, Mairéad G., Jean-Yves Scoazec, and Thomas Walter. "Extrapulmonary poorly differentiated NECs, including molecular and immune aspects." Endocrine-Related Cancer 27, no. 7 (July 2020): R219—R238. http://dx.doi.org/10.1530/erc-19-0483.

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Patients with extrapulmonary poorly differentiated neuroendocrine carcinomas (EP-PD-NECs) have a poor prognosis. Surgery is offered for those with localised disease, but the majority of patients present with advanced disease. Treatment strategies adopted are analogous to that of high grade NECs of the lung, with platinum/etoposide-based regimens advocated in the first-line setting for advanced disease. There is no standard second-line therapy. Research into their molecular and immune pathways may pave the way for novel drug discovery. The molecular drivers of NEC are best identified in small cell lung carcinoma, which present with near universal genomic alterations in TP53 and RB1. The genetics of EP-PD-NEC remain poorly understood; TP53, KRAS, PIK3CA/PTEN and BRAF mutations have been identified, with alterations in the BRCA pathway reported additionally in small cell NEC of the cervix and absence of argininosuccinate synthetase 1 expression in NEC of the urinary bladder. The use of cell lines and patient-derived xenografts (PDX) to predict response to treatment in NEC and the emergence of alternative biomarkers, such as circulating tumour cells and cell-free DNA, will also be explored. Despite limited published data on the immune microenvironment of EP-NEC, there are a number of clinical trials investigating the use of immune-targeted agents in this disease category, with conflicting emerging data from studies thus far. This review will summarise the treatment and available molecular and immune data in this under researched diagnosis and may stimulate the direction of future exploratory studies.

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de Vries, Stefan P. W., Hester J. Bootsma, John P. Hays, and Peter W. M. Hermans. "Molecular Aspects of Moraxella catarrhalis Pathogenesis." Microbiology and Molecular Biology Reviews 73, no. 3 (September 2009): 389–406. http://dx.doi.org/10.1128/mmbr.00007-09.

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SUMMARY In recent years, Moraxella catarrhalis has established its position as an important human mucosal pathogen, no longer being regarded as just a commensal bacterium. Further, current research in the field has led to a better understanding of the molecular mechanisms involved in M. catarrhalis pathogenesis, including mechanisms associated with cellular adherence, target cell invasion, modulation of the host's immune response, and metabolism. Additionally, in order to be successful in the host, M. catarrhalis has to be able to interact and compete with the commensal flora and overcome stressful environmental conditions, such as nutrient limitation. In this review, we provide a timely overview of the current understanding of the molecular mechanisms associated with M. catarrhalis virulence and pathogenesis.

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Zav'Yalov, VLADIMIR P., ALEXANDER I. Denesyuk, JUHANI Lundell, and TIMO Korpela. "Some new aspects of molecular mechanisms of cyclosporin A effect on immune response." APMIS 103, no. 1-6 (January 1995): 401–15. http://dx.doi.org/10.1111/j.1699-0463.1995.tb01125.x.

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Robinson, John A., and Kerstin Moehle. "Structural aspects of molecular recognition in the immune system. Part II: Pattern recognition receptors (IUPAC Technical Report)." Pure and Applied Chemistry 86, no. 10 (October 21, 2014): 1483–538. http://dx.doi.org/10.1515/pac-2013-1026.

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Abstract The vertebrate immune system uses pattern recognition receptors (PRRs) to detect a large variety of molecular signatures (pathogen-associated molecular patterns, PAMPs) from a broad range of different invading pathogens. The PAMPs range in size from relatively small molecules, to others of intermediate size such as bacterial lipopolysaccharide, lipopeptides, and oligosaccharides, to macromolecules such as viral DNA, RNA, and pathogen-derived proteins such as flagellin. Underlying this functional diversity of PRRs is a surprisingly small number of structurally distinct protein folds that include leucine-rich repeats in Toll-like receptors (TLRs) and NOD-like receptors (NLRs), the DExH box helicase domain in RIG-like receptors (RLRs), and C-type lectin domains (CTLDs) in the C-type lectins. Following PAMP recognition by the PRRs, downstream signaling pathways activate the innate immune system to respond to invading pathogenic organisms. The resulting stimulatory response is also vital for a balanced adaptive immune response to the pathogen, mediated by circulating antibodies and/or cytotoxic T cells. However, an aberrant stimulation of the innate immune system can also lead to excessive inflammatory and toxic stress responses. Exciting opportunities are now arising for the design of small synthetic molecules that bind to PRRs and influence downstream signaling pathways. Such molecules can be useful tools to modulate immune responses, for example, as adjuvants to stimulate adaptive immune responses to a vaccine, or as therapeutic agents to dampen aberrant immune responses, such as inflammation. The design of agonists or antagonists of PRRs can now benefit from a surge in knowledge of the 3D structures of PRRs, many in complexes with their natural ligands. This review article describes recent progress in structural studies of PRRs (TLRs, NLRs, CTLs, and RLRs), which is required for an understanding of how they specifically recognize structurally diverse “foreign” PAMPs amongst a background of other “self” molecules, sometimes closely related in structure, that are present in the human body.

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Cohen-Inbar, Or, and Menashe Zaaroor. "Immunological Aspects of Malignant Gliomas." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 43, no. 4 (April 13, 2016): 494–502. http://dx.doi.org/10.1017/cjn.2016.34.

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AbstractGlioblastoma Multiforme (GBM) is the most common malignant primary brain neoplasm having a mean survival time of <24 months. This figure remains constant, despite significant progress in medical research and treatment. The lack of an efficient anti-tumor immune response and the micro-invasive nature of the glioma malignant cells have been explained by a multitude of immune-suppressive mechanisms, proven in different models. These immune-resistant capabilities of the tumor result in a complex interplay this tumor shares with the immune system. We present a short review on the immunology of GBM, discussing the different unique pathological and molecular features of GBM, current treatment modalities, the principles of cancer immunotherapy and the link between GBM and melanoma. Current knowledge on immunological features of GBM, as well as immunotherapy past and current clinical trials, is discussed in an attempt to broadly present the complex and formidable challenges posed by GBM.

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Teras, Jüri, Michael J. Carr, Jonathan S. Zager, and Hidde M. Kroon. "Molecular Aspects of the Isolated Limb Infusion Procedure." Biomedicines 9, no. 2 (February 7, 2021): 163. http://dx.doi.org/10.3390/biomedicines9020163.

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For decades, isolated limb infusion (ILI) and hyperthermic isolated limb perfusion (HILP) have been used to treat melanoma in-transit metastases and unresectable sarcoma confined to the limb utilizing the effect of loco-regional high-dose chemotherapy to the isolated limb. Both procedures are able to provide high response rates in patients with numerous or bulky lesions in whom other loco-regional treatments are becoming ineffective. In comparison to systemic therapies, on the other hand, ILI and HILP have the advantage of not being associated with systemic side-effects. Although in principle ILI and HILP are similar procedures, ILI is technically simpler to perform and differs from HILP in that it takes advantage of the hypoxic and acidotic environment that develops in the isolated limb, potentiating anti-tumour activity of the cytotoxic agents melphalan +/− actinomycin-D. Due to its simplicity, ILI can be used in both preclinical and clinical studies to test new cytotoxic regimens and combinations with the aim to overcome tumour resistance. In the future, administration of cytotoxic agents by ILI, in combination with systemic treatments such as BRAF/MEK/KIT inhibitors, immunotherapy (CTLA-4 blockade), and/or programmed death (PD-1) pathway inhibitors, has the potential to improve responses further by inducing increased tumour cell death while limiting the ability of the tumour to suppress the immune response.

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Kalaria, R. N., M. Harshbarger-Kelly, D. L. Cohen, and D. R. D. Premkumar. "Molecular aspects of inflammatory and immune responses in Alzheimer's disease." Neurobiology of Aging 17, no. 5 (September 1996): 687–93. http://dx.doi.org/10.1016/0197-4580(96)00114-5.

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Nedoszytko, Bogusław, Edyta Reszka, Danuta Gutowska-Owsiak, Magdalena Trzeciak, Magdalena Lange, Justyna Jarczak, Marek Niedoszytko, et al. "Genetic and Epigenetic Aspects of Atopic Dermatitis." International Journal of Molecular Sciences 21, no. 18 (September 4, 2020): 6484. http://dx.doi.org/10.3390/ijms21186484.

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Atopic dermatitis is a heterogeneous disease, in which the pathogenesis is associated with mutations in genes encoding epidermal structural proteins, barrier enzymes, and their inhibitors; the role of genes regulating innate and adaptive immune responses and environmental factors inducing the disease is also noted. Recent studies point to the key role of epigenetic changes in the development of the disease. Epigenetic modifications are mainly mediated by DNA methylation, histone acetylation, and the action of specific non-coding RNAs. It has been documented that the profile of epigenetic changes in patients with atopic dermatitis (AD) differs from that observed in healthy people. This applies to the genes affecting the regulation of immune response and inflammatory processes, e.g., both affecting Th1 bias and promoting Th2 responses and the genes of innate immunity, as well as those encoding the structural proteins of the epidermis. Understanding of the epigenetic alterations is therefore pivotal to both create new molecular classifications of atopic dermatitis and to enable the development of personalized treatment strategies.

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Kubistova, Zuzana, Frantisek Mrazek, and Martin Petrek. "POLYMORPHISMS OF THE IMMUNE RESPONSE GENES:SELECTED BIOLOGICAL, METHODICAL AND MEDICAL ASPECTS." Biomedical Papers 153, no. 2 (June 1, 2009): 93–102. http://dx.doi.org/10.5507/bp.2009.016.

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Baugh, JA, and SC Donnelly. "Macrophage migration inhibitory factor: a neuroendocrine modulator of chronic inflammation." Journal of Endocrinology 179, no. 1 (October 1, 2003): 15–23. http://dx.doi.org/10.1677/joe.0.1790015.

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The diverse actions of macrophage migration inhibitory factor (MIF) within the immuno-neuroendocrine system are yet to be fully understood, but it is clear that MIF plays a pivotal role in the regulation of both the innate and adaptive immune response. An emerging body of data presently indicates that MIF's position within the cytokine cascade is to act in concert with glucocorticoids to control the 'set point' and magnitude of the immune and inflammatory response. In this article we will review the actions of MIF within the immune system and discuss the overlapping and contrasting aspects of MIF and glucocorticoid biology. In particular we will focus on the role of MIF within the immuno-neuroendocrine interface and suggest molecular mechanisms by which MIF may counter-regulate glucocorticoid function. Finally we will discuss emerging evidence that functional MIF gene-promoter polymorphisms render one susceptible to elevated MIF expression, and the development of an exaggerated immune/inflammatory response that potentiates the progression to chronic inflammatory disease.

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Al Hadra, Bushra N. "Some of the Immunogenetics Aspects of Aging." Journal of Biomedical and Clinical Research 14, no. 1 (June 1, 2021): 16–30. http://dx.doi.org/10.2478/jbcr-2021-0003.

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Summary The human life span could be influenced by the combined effect of environment, lifestyle, and genetic factors. Twin and family studies suggest that our genes control up to 25% of the lifespan. The aging immune system undergoes age-associated changes at multiple levels, resulting in a gradual loss of its ability to protect the organism against infections, low vaccine responses, and an increased probability of developing autoimmune diseases and malignancies. The highly polymorphic HLA complex is one of the major gene candidates associated with aging due to its crucial role in developing adaptive immunity and protecting the organism. Most of the data available have so far demonstrated a positive association with healthy aging for HLA alleles/haplotypes as protective against malignancies, autoimmune diseases, and conferring better control and response to infections. One of aging’s main manifestations is the chronic, low-grade inflammatory state observed in older people, caused by an imbalance between pro- and anti-inflammatory cytokines. In general, it is has been agreed that longevity is related to anti-inflammatory genotype profiles. With advanced age, changes also occur in the B cell repertoire, which significantly affects the humoral immunity and leads to inadequate responses to infections and vaccines in the elderly. New genetic biomarkers associated with aging are being explored and discovered, contributing to a better understanding of the molecular processes underlying the immune dysfunction related to aging and developing strategies for rejuvenating the immune system based on immune-risk phenotypes.

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Kaye, Paul M. "Molecular aspects of immune response and infectious diseases (Advances in Host Defense Mechanisms, vol. 7)." Parasitology Today 7, no. 7 (January 1991): 187. http://dx.doi.org/10.1016/0169-4758(91)90131-7.

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Wumba, R., M. Mandina, Y. Nlandu, J. R. Makulo, A. Tshimpi, P. Mbala, A. Mbangama, P. Kabututu, and J. M. Kayembe. "SARS-CoV-2: Molecular Structure, Pathogenesis, Potential Therapeutic Targets, and Immune Response of the Infected Subject." Interdisciplinary Perspectives on Infectious Diseases 2022 (June 2, 2022): 1–10. http://dx.doi.org/10.1155/2022/7856659.

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Background. The pathogenic mechanisms and immune response of COVID-19 are far from clear. Through a documentary review of literature, the authors describe virological and molecular aspects of SARS-CoV-2, the intimate mechanisms of cell infection, and potential therapeutic targets. They also analyze the characteristics of immune response of the infected subject. Objectives. Objectives of this study are to describe the state of knowledge on virological data, molecular and physiopathogenic mechanisms of SARS-CoV-2, with a view to a better understanding of the therapeutic targets, as well as the immune response of the infected subject. Methodology. This documentary review is a compilation of several meta-analyses, consistent with the methodology described in the PRISMA statement on literature data on SARS-CoV-2, published between March 22 and August 14, 2020 (Moher et al.). The search engines used for the selection of articles were as follows: PubMed, Google Scholar, Global Health, and WHO reports. Papers of interest were those addressing virological and molecular data on SARS-CoV-2, therapeutic aspects of COVID-19, and immunity of the infected subject. Of the 617 eligible papers, 417 could be retained after removing the duplicates. Ultimately, only 50 articles were retained for final evaluation. The data collected allowed the development of a two-armed model around the physiopathological aspects and potential therapeutic targets, as well as aspects of host immunity, respectively. The model was then compared to data from the HIV literature. Conclusion. Reported data could contribute to a better understanding of molecular mechanisms of cellular infection by SARS-CoV-2 as well as to a more easy explanation of the action of pharmacological agents used for the treatment, while elucidating intimate mechanisms of the immunity of infected subject.

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Buldain, Idoia, Leire Martin-Souto, Aitziber Antoran, Maialen Areitio, Leire Aparicio-Fernandez, Aitor Rementeria, Fernando L. Hernando, and Andoni Ramirez-Garcia. "The Host Immune Response to Scedosporium/Lomentospora." Journal of Fungi 7, no. 2 (January 22, 2021): 75. http://dx.doi.org/10.3390/jof7020075.

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Infections caused by the opportunistic pathogens Scedosporium/Lomentospora are on the rise. This causes problems in the clinic due to the difficulty in diagnosing and treating them. This review collates information published on immune response against these fungi, since an understanding of the mechanisms involved is of great interest in developing more effective strategies against them. Scedosporium/Lomentospora cell wall components, including peptidorhamnomannans (PRMs), α-glucans and glucosylceramides, are important immune response activators following their recognition by TLR2, TLR4 and Dectin-1 and through receptors that are yet unknown. After recognition, cytokine synthesis and antifungal activity of different phagocytes and epithelial cells is species-specific, highlighting the poor response by microglial cells against L. prolificans. Moreover, a great number of Scedosporium/Lomentospora antigens have been identified, most notably catalase, PRM and Hsp70 for their potential medical applicability. Against host immune response, these fungi contain evasion mechanisms, inducing host non-protective response, masking fungal molecular patterns, destructing host defense proteins and decreasing oxidative killing. In conclusion, although many advances have been made, many aspects remain to be elucidated and more research is necessary to shed light on the immune response to Scedosporium/Lomentospora.

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Quirino, Angela, Nadia Marascio, Giorgio Settimo Barreca, Luigia Gallo, Aida Giancotti, Angelo Giuseppe Lamberti, Cinzia Peronace, et al. "SARS-CoV-2: Some Aspects of Molecular Evolution, Cellular Pathogenesis, and Immune System Mechanism Elusion." Applied Sciences 11, no. 24 (December 7, 2021): 11605. http://dx.doi.org/10.3390/app112411605.

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The purpose of this review is to address some of the latest aspects regarding molecular features, pathogenic mechanisms, and immune system response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), based on recent publications in this field from March 2020 to May 2021. Interpretation keys for periodic re-emergence of coronavirus infections and other lethal viral pandemics are suggested. Antibody-dependent enhancement (ADE) and other potential mechanisms of immune system deception are put forward. Therefore, vaccine development must take into account ADE and other unwanted side effects of immune-based medical intervention. Features reported in our review will allow both clinicians and basic science researchers to take home ideas to improve their knowledge about SARS-CoV-2.

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Ribarac-Stepic, Nevena, Snezana Djurica, Zorica Zakula, Goran Koricanac, and Dragoslav Milosevic. "Molecular basis of glucocorticoid action." Srpski arhiv za celokupno lekarstvo 133, Suppl. 1 (2005): 61–66. http://dx.doi.org/10.2298/sarh05s1061r.

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Glucocorticoid hormones are involved in regulation of cell processes and coordinate physiological response to diverse signals. These hormones, through interaction with specific intracellular receptors, coordinate components of physiological repertoires by activating the expression of gene networks. Thus hormone-receptor complexes may function as key constituent in regulation of specific cell functions as well as in provoking differentiation in already determined cells. Analysis of steroid receptors are important for understanding of molecular details of transcriptional control as well as providing the insight as to how an individual transcriptional factor such as glucocorticoid receptor, contributes to cell identity and function. The purpose of this review is to establish the general molecular mechanism of glucocorticoid action and mechanism associated hormonereceptor complexes with the control of differential patterns (i.e. ?positive? and ?negative?) of gene expression. One of the examples of two signal pathways regulating opposite gene expression are NF-?B and GR-mediated signal pathways. These pathways have important and opposite roles in the immune function. NF-?B is transcription factor which induces the expression of many genes that participate in immune and inflamatory response, while GR is transcription factor that serves as antiinflammatory agent and immune suppressor. Their interactions within the cell, although not yet completely understood, appear to be an important, possibly even the primary mechanism of immune homeostasis. It has not been established that glucocorticoid sensitivity can be caused by mechanisms other than changes of GR number and properties, although recent studies have indicated that receptor isoforms and transcriptional factors may modulate glucocorticoid responsiveness by interacting with receptor protein or directly at the site of DNA binding. The aim of this review is also to describe the role of glucocorticoid receptors in mechanism of glucocorticoid action on cell functions, including immune responses, as well as to present emerging issues on clinical aspects of molecular mechanisms of glucocorticoid action.

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Galeas-Pena, Michelle, Nathaniel McLaughlin, and Derek Pociask. "The role of the innate immune system on pulmonary infections." Biological Chemistry 400, no. 4 (April 24, 2019): 443–56. http://dx.doi.org/10.1515/hsz-2018-0304.

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Abstract Inhalation is required for respiration and life in all vertebrates. This process is not without risk, as it potentially exposes the host to environmental pathogens with every breath. This makes the upper respiratory tract one of the most common routes of infection and one of the leading causes of morbidity and mortality in the world. To combat this, the lung relies on the innate immune defenses. In contrast to the adaptive immune system, the innate immune system does not require sensitization, previous exposure or priming to attack foreign particles. In the lung, the innate immune response starts with the epithelial barrier and mucus production and is reinforced by phagocytic cells and T cells. These cells are vital for the production of cytokines, chemokines and anti-microbial peptides that are critical for clearance of infectious agents. In this review, we discuss all aspects of the innate immune response, with a special emphasis on ways to target aspects of the immune response to combat antibiotic resistant bacteria.

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Dolmatov, Igor Yu. "Molecular Aspects of Regeneration Mechanisms in Holothurians." Genes 12, no. 2 (February 10, 2021): 250. http://dx.doi.org/10.3390/genes12020250.

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Holothurians, or sea cucumbers, belong to the phylum Echinodermata. They show good regenerative abilities. The present review provides an analysis of available data on the molecular aspects of regeneration mechanisms in holothurians. The genes and signaling pathways activated during the asexual reproduction and the formation of the anterior and posterior parts of the body, as well as the molecular mechanisms that provide regeneration of the nervous and digestive systems, are considered here. Damage causes a strong stress response, the signs of which are recorded even at late regeneration stages. In holothurian tissues, the concentrations of reactive oxygen species and antioxidant enzymes increase. Furthermore, the cellular and humoral components of the immune system are activated. Extracellular matrix remodeling and Wnt signaling play a major role in the regeneration in holothurians. All available morphological and molecular data show that the dedifferentiation of specialized cells in the remnant of the organ and the epithelial morphogenesis constitute the basis of regeneration in holothurians. However, depending on the type of damage, the mechanisms of regeneration may differ significantly in the spatial organization of regeneration process, the involvement of different cell types, and the depth of reprogramming of their genome (dedifferentiation or transdifferentiation).

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Jacobs, Andreas H., and Bertrand Tavitian. "Noninvasive Molecular Imaging of Neuroinflammation." Journal of Cerebral Blood Flow & Metabolism 32, no. 7 (May 2, 2012): 1393–415. http://dx.doi.org/10.1038/jcbfm.2012.53.

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Inflammation is a highly dynamic and complex adaptive process to preserve and restore tissue homeostasis. Originally viewed as an immune-privileged organ, the central nervous system (CNS) is now recognized to have a constant interplay with the innate and the adaptive immune systems, where resident microglia and infiltrating immune cells from the periphery have important roles. Common diseases of the CNS, such as stroke, multiple sclerosis (MS), and neurodegeneration, elicit a neuroinflammatory response with the goal to limit the extent of the disease and to support repair and regeneration. However, various disease mechanisms lead to neuroinflammation (NI) contributing to the disease process itself. Molecular imaging is the method of choice to try to decipher key aspects of the dynamic interplay of various inducers, sensors, transducers, and effectors of the orchestrated inflammatory response in vivo in animal models and patients. Here, we review the basic principles of NI with emphasis on microglia and common neurologic disease mechanisms, the molecular targets which are being used and explored for imaging, and molecular imaging of NI in frequent neurologic diseases, such as stroke, MS, neurodegeneration, epilepsy, encephalitis, and gliomas.

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Canisso, Igor F., Lorenzo G. T. M. Segabinazzi, and Carleigh E. Fedorka. "Persistent Breeding-Induced Endometritis in Mares—A Multifaceted Challenge: From Clinical Aspects to Immunopathogenesis and Pathobiology." International Journal of Molecular Sciences 21, no. 4 (February 20, 2020): 1432. http://dx.doi.org/10.3390/ijms21041432.

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Post-breeding endometritis (i.e., inflammation/infection of the endometrium), is a physiological reaction taking place in the endometrium of mares within 48 h post-breeding, aimed to clear seminal plasma, excess sperm, microorganisms, and debris from the uterine lumen in preparation for the arrival of an embryo. Mares are classified as susceptible or resistant to persistent breeding-induced endometritis (PBIE) based on their ability to clear this inflammation/infection by 48 h post-breeding. Mares susceptible to PBIE, or those with difficulty clearing infection/inflammation, have a deficient immune response and compromised physical mechanisms of defense against infection. Molecular pathways of the innate immune response known to be involved in PBIE are discussed herein. The role of the adaptive uterine immune response on PBIE remains to be elucidated in horses. Advances in the pathobiology of microbes involved in PBIE are also revised here. Traditional and non-traditional therapeutic modalities for endometritis are contrasted and described in the context of clinical and molecular aspects. In recent years, the lack of efficacy of traditional therapeutic modalities, alongside the ever-increasing incidence of antibiotic-resistant microorganisms, has enforced the development of non-traditional therapies. Novel biological products capable of modulating the endometrial inflammatory response are also discussed here as part of the non-traditional therapies for endometritis.

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Ramon-Patino, Jorge Luis, Sabine Schmid, Sally Lau, Lesley Seymour, Pierre-Olivier Gaudreau, Janice Juan Ning Li, Penelope Ann Bradbury, and Emiliano Calvo. "iRECIST and atypical patterns of response to immuno-oncology drugs." Journal for ImmunoTherapy of Cancer 10, no. 6 (June 2022): e004849. http://dx.doi.org/10.1136/jitc-2022-004849.

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With the advent of immunotherapy as one of the keystones of the treatment of our patients with cancer, a number of atypical patterns of response to these agents has been identified. These include pseudoprogression, where the tumor initially shows objective growth before decreasing in size, and hyperprogression, hypothesized to be a drug-induced acceleration of the tumor burden. Despite it being >10 years since the first immune-oncology drug was approved, neither the biology behind these paradoxical responses has been well understood, nor their incidence, identification criteria, predictive biomarkers, or clinical impact have been fully described. Immune-based Response Evaluation Criteria in Solid Tumors (iRECIST) guidelines have been published as a revision to the RECIST V.1.1 criteria for use in trials of immunotherapeutics, and the iRECIST subcommittee (of the RECIST Working Group) is working on elucidating these aspects, with data sharing a current major challenge to move forward with this unmet need in immuno-oncology.

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31

Esteves, Eduardo, Vera M. Mendes, Bruno Manadas, Rafaela Lopes, Liliana Bernardino, Maria José Correia, Marlene Barros, Ana Cristina Esteves, and Nuno Rosa. "COVID-19 Salivary Protein Profile: Unravelling Molecular Aspects of SARS-CoV-2 Infection." Journal of Clinical Medicine 11, no. 19 (September 22, 2022): 5571. http://dx.doi.org/10.3390/jcm11195571.

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COVID-19 is the most impacting global pandemic of all time, with over 600 million infected and 6.5 million deaths worldwide, in addition to an unprecedented economic impact. Despite the many advances in scientific knowledge about the disease, much remains to be clarified about the molecular alterations induced by SARS-CoV-2 infection. In this work, we present a hybrid proteomics and in silico interactomics strategy to establish a COVID-19 salivary protein profile. Data are available via ProteomeXchange with identifier PXD036571. The differential proteome was narrowed down by the Partial Least-Squares Discriminant Analysis and enrichment analysis was performed with FunRich. In parallel, OralInt was used to determine interspecies Protein-Protein Interactions between humans and SARS-CoV-2. Five dysregulated biological processes were identified in the COVID-19 proteome profile: Apoptosis, Energy Pathways, Immune Response, Protein Metabolism and Transport. We identified 10 proteins (KLK 11, IMPA2, ANXA7, PLP2, IGLV2-11, IGHV3-43D, IGKV2-24, TMEM165, VSIG10 and PHB2) that had never been associated with SARS-CoV-2 infection, representing new evidence of the impact of COVID-19. Interactomics analysis showed viral influence on the host immune response, mainly through interaction with the degranulation of neutrophils. The virus alters the host’s energy metabolism and interferes with apoptosis mechanisms.

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Zhdanov, Vladimir P. "Spatio-temporal aspects of the interplay of cancer and the immune system." Journal of Biological Physics 45, no. 4 (November 26, 2019): 395–400. http://dx.doi.org/10.1007/s10867-019-09535-3.

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AbstractThe conventional mean-field kinetic models describing the interplay of cancer and the immune system are temporal and predict exponential growth or elimination of the population of tumour cells provided their number is small and their effect on the immune system is negligible. More complex kinetics are associated with non-linear features of the response of the immune system. The generic model presented in this communication takes into account that the rates of the birth and death of tumour cells inside a tumour spheroid can significantly depend on the radial coordinate due to diffusion limitations in the supply of nutrients and/or transport of the species (cells and proteins) belonging to the immune system. In this case, non-trivial kinetic regimes are shown to be possible even without appreciable perturbation of the immune system.

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Nakaghi, Andréa Cristina Higa, Rosangela Zacarias Machado, Mirela Tinucci Costa, Marcos Rogério André, and Cristiane Divan Baldani. "Canine ehrlichiosis: clinical, hematological, serological and molecular aspects." Ciência Rural 38, no. 3 (June 2008): 766–70. http://dx.doi.org/10.1590/s0103-84782008000300027.

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The aim of the present study was to compare the direct detection methods of Ehrlichia canis (blood smears and nested PCR), serological tests (Dot-ELISA and Immunofluorescent Antibody Test - IFAT), and demonstrate the most suitable test for the diagnosis of different stages of infection. Blood samples and clinical data were collected from 30 dogs examined at the Veterinary Teaching Hospital, UNESP, Jaboticabal, SP, Brazil. The clinical signs most frequently observed were apathy, anorexia, pale mucous membrane, fever, lymphadenopathy, splenomegaly, hemorrhages and uveitis. Evaluating the humoral immune response, 63.3% of the sera were IFAT positive, while 70% were Dot-ELISA positive. By nestedPCR 53.3% of the samples were positive. Comparing these techniques it was concluded that serology and nPCR are the most suitable tests to confirm the diagnosis of canine ehrlichiosis, however it should be always treated as a complementary data to clinical and hematological evaluation. Serology has an important role in the subclinical and in the chronic phase, nPCR is recommended in the acute stage, and, especially, to identify the ehrlichia specie.

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Bernstein, Kenneth E., Romer A. Gonzalez-Villalobos, Jorge F. Giani, Kandarp Shah, Ellen Bernstein, Tea Janjulia, Yosef Koronyo, et al. "Angiotensin-converting enzyme overexpression in myelocytes enhances the immune response." Biological Chemistry 395, no. 10 (October 1, 2014): 1173–78. http://dx.doi.org/10.1515/hsz-2013-0295.

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Abstract Angiotensin-converting enzyme (ACE) plays an important role in blood pressure control. ACE also has effects on renal function, reproduction, hematopoiesis, and several aspects of the immune response. ACE 10/10 mice overexpress ACE in monocytic cells; macrophages from ACE 10/10 mice demonstrate increased polarization toward a proinflammatory phenotype. As a result, ACE 10/10 mice have a highly effective immune response following challenge with melanoma, bacterial infection, or Alzheimer disease. As shown in ACE 10/10 mice, enhanced monocytic function greatly contributes to the ability of the immune response to defend against a wide variety of antigenic and non-antigenic challenges.

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35

Andalib, Ali Reza, and Maedeh Radandish. "Immunological and Clinical Aspects of Immune Responses to SARS-CoV-2." Journal of Qazvin University of Medical Sciences 24, no. 6 (February 1, 2020): 592–613. http://dx.doi.org/10.32598/jqums.24.6.10.

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The Coronavirus Disease 2019 (COVID-19) caused by a coronavirus named SARS-CoV-2 from the family Coronaviridae, was first reported in December 2019 in China. The disease have mild or severe symptoms such as fever, chills, cough, shortness of breath, body aches, and gastrointestinal symptoms, followed by severe inflammation, cytokine storm, acute respiratory distress syndrome, and dysfunction of other organs. In this narrative review study, the search was conducted on related studies published during January- October 2020 in Google Scholar, PubMed, Embase, and Scopus databases using the keywords Covid-19, Immunology, and Immunopathogenesis. Among abundant and mostly repetitive information, the immunological aspects were selected. The SARS-CoV-2 can enter the cell by binding to the Angiotensin-Converting Enzyme 2 (ACE2) receptor and Trans-Membrane Protease Serine 2 (TMPRSS2) on the surface of lung epithelial cells. The main pathogenic mechanism of infection with SARS-CoV-2 is the stimulation of inflammatory response followed by damage to the alveoli of lung tissue. In uncontrolled immune responses, the infiltration of macrophages, monocytes, neutrophils, and inflammatory T cells into the alveoli increases which leads to tissue damage in the lungs and other organs by overproduction of inflammatory cytokines such as Interleukin 6 (IL-6), Tumor Necrosis Factor alpha (TNF-α), Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF), Interleukin 6 (IL-8), Interferon gamma (IFNγ), etc. The Natural Killer (NK) and T cell dysfunction, lymphopenia, and infection of immune cells such as monocytes with ADE mechanism are factors causing the body’s failure in resistance to SARS-CoV-2 virus. Diagnosis of COVID-19 is based on the clinical symptoms and the results of molecular tests (e.g. Polymerase Chain Reaction test), or computerized tomography scan followed by serological tests and measuring biochemical factors in the blood (e.g. lymphocyte count, C-reactive protein, dimerized plasmin fragment D, etc.). Due to the association of the severity of COVID-19 with the uncontrolled immune response of the host, targeting any of the immunopathological pathways to inhibit inflammatory responses can be considered as potential therapeutic goals. The use of immune system regulators such as chloroquine, corticosteroids, inflammatory cytokine blockers such as anti-IL-6, anti-IL-1, and cell therapy at the right time have an enhanced effect on the recovery of the disease or inhibit the disease progression.

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Tomela, Katarzyna, Bernadeta Pietrzak, Marcin Schmidt, and Andrzej Mackiewicz. "The Tumor and Host Immune Signature, and the Gut Microbiota as Predictive Biomarkers for Immune Checkpoint Inhibitor Response in Melanoma Patients." Life 10, no. 10 (September 25, 2020): 219. http://dx.doi.org/10.3390/life10100219.

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There are various melanoma treatment strategies that are based on immunological responses, among which immune checkpoint inhibitors (ICI) are relatively novel form. Nowadays, anti-cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and anti-programmed death-1 (PD-1) antibodies represent a standard treatment for metastatic melanoma. Although there are remarkable curative effects in responders to ICI therapy, up to 70% of melanoma patients show resistance to this treatment. This low response rate is caused by innate as well as acquired resistance, and some aspects of treatment resistance are still unknown. Growing evidence shows that gut microbiota and bacterial metabolites, such as short-chain fatty acids (SCFAs), affect the efficacy of immunotherapy. Various bacterial species have been indicated as potential biomarkers of anti-PD-1 or anti-CTLA-4 therapy efficacy in melanoma, next to biomarkers related to molecular and genetic tumor characteristics or the host immunological response, which are detected in patients’ blood. Here, we review the current status of biomarkers of response to ICI melanoma therapies, their pre-treatment predictive values, and their utility as on-treatment monitoring tools in order to select a relevant personalized therapy on the basis of probability of the best clinical outcome.

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37

Boštjančič, Emanuela, Željka Večerić-Haler, and Nika Kojc. "The Role of Immune-Related miRNAs in the Pathology of Kidney Transplantation." Biomolecules 11, no. 8 (August 12, 2021): 1198. http://dx.doi.org/10.3390/biom11081198.

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MicroRNAs (miRNAs) are members of the non-coding regulatory RNA family that play pivotal roles in physiological and pathological conditions, including immune response. They are particularly interesting as promising therapeutic targets, prognostic and diagnostic markers due to their easy detection in body fluids and stability. There is accumulating evidence that different miRNAs provide disease-specific signatures in liquid samples of distinct kidney injuries. Using experimental models and human samples, there have been numerous suggestions that immune-related miRNAs are also important contributors to the development of different kidney diseases as well as important markers for monitoring response after kidney transplantation. However, there are limited data for understanding their function in the molecular pathways of allograft pathologies. In our review, we focused on microRNAs that are related to different aspects of immune response after kidney transplantation.

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Benayoun, Bérénice. "SEX-DIMORPHIC REGULATION OF INNATE IMMUNITY DURING AGING." Innovation in Aging 6, Supplement_1 (November 1, 2022): 165. http://dx.doi.org/10.1093/geroni/igac059.657.

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Abstract Aging is accompanied by striking changes in chromatin and gene expression across cell types and species. Yet, how chromatin landscapes change with age and regulate transcription, and how epigenomic changes in turn influence aging in response to external or internal cues, is largely unknown. In addition, accumulating evidence indicates that sex hormones play a key role in driving aspects of cellular and molecular sex-dimorphism. In parallel to sex hormones, karyotypic sex (i.e. XX vs. XY) is also likely to have important impact outside of gonadal sex determination. A key compartment whose activity can be actively modulated by sex-dimorphic mechanisms throughout life is the immune system, whose function declines sharply with aging and may be actively modulated by sex. Indeed, aspects of the immune responses differ between sexes, with a more robust immune response in females and an increased susceptibility to infection in males. Thus, our main cell models of study are key components of the innate immune system and the inflammatory response: macrophages, which accomplish key tasks such as phagocytosis, antigen presentation and cytokine production, and neutrophils, the most abundant leukocyte type serving as a “first line of defense” against infection. Excitingly, we and others have observed strong sex-related differences in the transcriptional and functional phenotypes of these cells and have observed sex-dimorphic “omic” trajectories for these cells with aging. Based on our data and published literature, it is likely that mechanisms involving both gonadal hormones and sex chromosomes may fine-tune different aspects of immunity and, thus, overall health and lifespan.

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Aldhamen, Yasser A., Sergey S. Seregin, David P. W. Rastall, Charles F. Aylsworth, Yuliya Pepelyayeva, Christopher J. Busuito, Sarah Godbehere-Roosa, Sungjin Kim, and Andrea Amalfitano. "Endoplasmic Reticulum Aminopeptidase-1 Functions Regulate Key Aspects of the Innate Immune Response." PLoS ONE 8, no. 7 (July 24, 2013): e69539. http://dx.doi.org/10.1371/journal.pone.0069539.

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40

Martí i Líndez, Adrià-Arnau, and Walter Reith. "Arginine-dependent immune responses." Cellular and Molecular Life Sciences 78, no. 13 (May 26, 2021): 5303–24. http://dx.doi.org/10.1007/s00018-021-03828-4.

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AbstractA growing body of evidence indicates that, over the course of evolution of the immune system, arginine has been selected as a node for the regulation of immune responses. An appropriate supply of arginine has long been associated with the improvement of immune responses. In addition to being a building block for protein synthesis, arginine serves as a substrate for distinct metabolic pathways that profoundly affect immune cell biology; especially macrophage, dendritic cell and T cell immunobiology. Arginine availability, synthesis, and catabolism are highly interrelated aspects of immune responses and their fine-tuning can dictate divergent pro-inflammatory or anti-inflammatory immune outcomes. Here, we review the organismal pathways of arginine metabolism in humans and rodents, as essential modulators of the availability of this semi-essential amino acid for immune cells. We subsequently review well-established and novel findings on the functional impact of arginine biosynthetic and catabolic pathways on the main immune cell lineages. Finally, as arginine has emerged as a molecule impacting on a plethora of immune functions, we integrate key notions on how the disruption or perversion of arginine metabolism is implicated in pathologies ranging from infectious diseases to autoimmunity and cancer.

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41

Ehlting, Christian, Stephanie D. Wolf, and Johannes G. Bode. "Acute-phase protein synthesis: a key feature of innate immune functions of the liver." Biological Chemistry 402, no. 9 (July 29, 2021): 1129–45. http://dx.doi.org/10.1515/hsz-2021-0209.

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Abstract The expression of acute-phase proteins (APP’s) maintains homeostasis and tissue repair, but also represents a central component of the organism’s defense strategy, especially in the context of innate immunity. Accordingly, an inflammatory response is accompanied by significant changes in the serum protein composition, an aspect that is also used diagnostically. As the main site of APP synthesis the liver is constantly exposed to antigens or pathogens via blood flow, but also to systemic inflammatory signals originating either from the splanchnic area or from the circulation. Under both homeostatic and acute-phase response (APR) conditions the composition of APP’s is determined by the pattern of regulatory mediators derived from the systemic circulation or from local cell populations, especially liver macrophages. The key regulators mentioned here most frequently are IL-1β, IL-6 and TNF-α. In addition to a variety of molecular mediators described mainly on the basis of in vitro studies, recent data emphasize the in vivo relevance of cellular key effectors as well as molecular key mediators and protein modifications for the regulation and function of APP’s. These are aspects, on which the present review is primarily focused.

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Siracusano, Alessandra, Federica Delunardo, Antonella Teggi, and Elena Ortona. "Host-Parasite Relationship in Cystic Echinococcosis: An Evolving Story." Clinical and Developmental Immunology 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/639362.

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The larval stage ofEchinococcus granulosuscauses cystic echinococcosis, a neglected infectious disease that constitutes a major public health problem in developing countries. Despite being under constant barrage by the immune system,E. granulosusmodulates antiparasite immune responses and persists in the human hosts with detectable humoral and cellular responses against the parasite.In vitroandin vivoimmunological approaches, together with molecular biology and immunoproteomic technologies, provided us exciting insights into the mechanisms involved in the initiation ofE. granulosusinfection and the consequent induction and regulation of the immune response. Although the last decade has clarified many aspects of host-parasite relationship in human cystic echinococcosis, establishing the full mechanisms that cause the disease requires more studies. Here, we review some of the recent developments and discuss new avenues in this evolving story ofE. granulosusinfection in man.

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Donn, RP, and DW Ray. "Macrophage migration inhibitory factor: molecular, cellular and genetic aspects of a key neuroendocrine molecule." Journal of Endocrinology 182, no. 1 (July 1, 2004): 1–9. http://dx.doi.org/10.1677/joe.0.1820001.

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The immunological and neuroendocrine properties of macrophage migration inhibitory factor (MIF) are diverse. In this article we review the known cellular, molecular and genetic properties of MIF that place it as a key regulatory cytokine, acting within both the innate and adaptive immune responses.The unexpected and paradoxical induction of MIF secretion by low concentrations of glucocorticoids is explored. The role of MIF as a locally acting modulator of glucocorticoid sensitivity within foci of inflammation is also discussed. MIF has no homology with any other pro-inflammatory cytokine and until recently lacked a recognised transmembrane receptor. MIF has also been shown to be directly taken up into target cells and to interact with intracellular signalling molecules, including the Jun activation domain-binding protein Jab-1.Comprehensive analysis of the MIF gene has identified important functional polymorphisms and a series of genetic studies has revealed both association and linkage of MIF with inflammatory diseases. Altered MIF regulation may therefore be pivotal to acquiring chronic inflammation following an innate immune response.

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Zhang, Wenbao, Hao Wen, Jun Li, Renyong Lin, and Donald P. McManus. "Immunology and Immunodiagnosis of Cystic Echinococcosis: An Update." Clinical and Developmental Immunology 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/101895.

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Cystic echinococcosis (CE) is a cosmopolitan zoonosis caused by the larval cystic stage of the dog tapewormEchinococcus granulosus. This complex multicellular pathogen produces various antigens which modulate the host immune response and promote parasite survival and development. The recent application of modern molecular and immunological approaches has revealed novel insights on the nature of the immune responses generated during the course of a hydatid infection, although many aspects of theEchinococcus-host interplay remain unexplored. This paper summarizes recent developments in our understanding of the immunology and diagnosis of echinococcosis, indicates areas where information is lacking, and suggests possible new strategies to improve serodiagnosis for practical application.

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Harding, Benjamin W., and Jonathan J. Ewbank. "An integrated view of innate immune mechanisms in C. elegans." Biochemical Society Transactions 49, no. 5 (October 8, 2021): 2307–17. http://dx.doi.org/10.1042/bst20210399.

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The simple notion ‘infection causes an immune response' is being progressively refined as it becomes clear that immune mechanisms cannot be understood in isolation, but need to be considered in a more global context with other cellular and physiological processes. In part, this reflects the deployment by pathogens of virulence factors that target diverse cellular processes, such as translation or mitochondrial respiration, often with great molecular specificity. It also reflects molecular cross-talk between a broad range of host signalling pathways. Studies with the model animal C. elegans have uncovered a range of examples wherein innate immune responses are intimately connected with different homeostatic mechanisms, and can influence reproduction, ageing and neurodegeneration, as well as various other aspects of its biology. Here we provide a short overview of a number of such connections, highlighting recent discoveries that further the construction of a fully integrated view of innate immunity.

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Warr, Alyson R., Carole J. Kuehl, and Matthew K. Waldor. "Shiga toxin remodels the intestinal epithelial transcriptional response to Enterohemorrhagic Escherichia coli." PLOS Pathogens 17, no. 2 (February 2, 2021): e1009290. http://dx.doi.org/10.1371/journal.ppat.1009290.

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Enterohemorrhagic Escherichia coli (EHEC) is a food-borne pathogen that causes diarrheal disease and the potentially lethal hemolytic uremic syndrome. We used an infant rabbit model of EHEC infection that recapitulates many aspects of human intestinal disease to comprehensively assess colonic transcriptional responses to this pathogen. Cellular compartment-specific RNA-sequencing of intestinal tissue from animals infected with EHEC strains containing or lacking Shiga toxins (Stx) revealed that EHEC infection elicits a robust response that is dramatically shaped by Stx, particularly in epithelial cells. Many of the differences in the transcriptional responses elicited by these strains were in genes involved in immune signaling pathways, such as IL23A, and coagulation, including F3, the gene encoding Tissue Factor. RNA FISH confirmed that these elevated transcripts were found almost exclusively in epithelial cells. Collectively, these findings suggest that Stx potently remodels the host innate immune response to EHEC.

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Zayats, Romaniya, Zhirong Mou, Atta Yazdanpanah, Wan Koh, Paul Lopez, Jude E. Uzonna, and Thomas Murooka. "Cellular dynamics of immune evasion during Leishmania major infection." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 75.6. http://dx.doi.org/10.4049/jimmunol.204.supp.75.6.

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Abstract Concomitant immunity against intracellular parasites is dictated by the immune response and parasite escape mechanisms that prevent clearance. Infection by Leishmania major generates a strong T cell response, yet parasite clearance is incomplete and leaves a small pool of persistently infected cells. T cell behaviours are augmented by the biochemical and spatial conditions of their immediate environments, and a gap in knowledge is the cellular and molecular mechanisms that prevent complete clearance of pathogen-infected cells in the skin. We combined MP-IVM with a novel T-cell receptor transgenic mouse model, where T cells recognize the immunodominant Leishmania-glycosomal phosphoenolpyruvate carboxykinase (PEPCK) peptide, to provide insights into the spatiotemporal dynamics of anti-Leishmania T cell responses during active disease and persistent infection. We show that monocyte-derived macrophage:T cell interaction dynamics were transient at steady-state, but prolonged upon antigen recognition. PEPCK-specific T cells produced high levels of IFNg in response to peptide or infection. We also show that in vitro expanded Treg cells can suppress effector T cell functions, and that greater suppression was observed by PEPCK-specific Treg cells. Ongoing studies that address the cellular and molecular mechanisms of Treg-mediated response blunting will be presented. Intravital microscopy studies characterizing PEPCK-specific T cell migration dynamics and tissue localization within skin lesions directly in live mice will also be presented. The goal of our study is to identify barriers to overcome in order to achieve complete parasite clearance and to better describe the dynamic aspects of concomitant immunity generation.

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48

Qin, Qingqing, Guangyao Li, Lian Jin, Yu Huang, Yu Wang, Chunhong Wei, Zhihong Xu, Zhirui Yang, Haiyang Wang, and Yi Li. "Auxin response factors (ARFs) differentially regulate rice antiviral immune response against rice dwarf virus." PLOS Pathogens 16, no. 12 (December 2, 2020): e1009118. http://dx.doi.org/10.1371/journal.ppat.1009118.

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There are 25 auxin response factors (ARFs) in the rice genome, which play critical roles in regulating myriad aspects of plant development, but their role (s) in host antiviral immune defense and the underneath mechanism remain largely unknown. By using the rice-rice dwarf virus (RDV) model system, here we report that auxin signaling enhances rice defense against RDV infection. In turn, RDV infection triggers increased auxin biosynthesis and accumulation in rice, and that treatment with exogenous auxin reduces OsIAA10 protein level, thereby unleashing a group of OsIAA10-interacting OsARFs to mediate downstream antiviral responses. Strikingly, our genetic data showed that loss-of-function mutants of osarf12 or osarf16 exhibit reduced resistance whereas osarf11 mutants display enhanced resistance to RDV. In turn, OsARF12 activates the down-stream OsWRKY13 expression through direct binding to its promoter, loss-of-function mutants of oswrky13 exhibit reduced resistance. These results demonstrated that OsARF 11, 12 and 16 differentially regulate rice antiviral defense. Together with our previous discovery that the viral P2 protein stabilizes OsIAA10 protein via thwarting its interaction with OsTIR1 to enhance viral infection and pathogenesis, our results reveal a novel auxin-IAA10-ARFs-mediated signaling mechanism employed by rice and RDV for defense and counter defense responses.

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TAN, Seng-Lai, and Peter J. PARKER. "Emerging and diverse roles of protein kinase C in immune cell signalling." Biochemical Journal 376, no. 3 (December 15, 2003): 545–52. http://dx.doi.org/10.1042/bj20031406.

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Members of the protein kinase C (PKC) family are expressed in many different cell types, where they are known to regulate a wide variety of cellular processes that impact on cell growth and differentiation, cytoskeletal remodelling and gene expression in the response to diverse stimuli. The broad tissue distribution and redundancy of in vitro function have often hampered the identification of definitive roles for each PKC family member. However, recent in vivo studies of PKC isoenzyme-selective knockout and transgenic mice have highlighted distinct functions of individual PKCs in the immune system. These genetic analyses, along with biochemical studies utilizing PKC isoenzyme-specific cDNA (wild-type, constitutively active and dominant-negative), antisense oligonucleotides (ASO), RNA interference (RNAi), and pharmacological inhibitors, indicate that PKC-regulated signalling pathways play a significant role in many aspects of immune responses, from development, differentiation, activation and survival of lymphocytes to macrophage activation. The importance of PKCs in cellular immune responses suggests that improved understanding of the molecular events that govern their actions could point to new avenues for development of treatments for immune disorders.

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50

Khammissa, R. A. G., R. Chandran, A. Masilana, J. Lemmer, and L. Feller. "Adverse Immunologically Mediated Oral Mucosal Reactions to Systemic Medication: Lichenoid Tissue Reaction/Interface Dermatitis-Stomatitis, Autoimmune Vesiculobullous Disease, and IgE-Dependent and Immune Complex Reactions." Journal of Immunology Research 2018 (June 10, 2018): 1–10. http://dx.doi.org/10.1155/2018/7645465.

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Drug-induced hypersensitivity immune reactions are exaggerated immunoinflammatory responses to allergenic components of the medications that occur in genetically susceptible subjects. The type of hypersensitivity immune response generated, whether antibody mediated or T cell mediated, or an immune complex reaction is determined by multiple factors, including the molecular characteristics of the allergen, the route of administration of the medication, the manner of presentation of the allergen by antigen-presenting cells to naïve T cells, the repertoire of the T cell receptors, and the cytokine profile within the microenvironment. This review deals with the clinical and histopathological aspects of adverse immunologically mediated oral mucosal reactions to systemic medication. We elaborate on diseases showing features of lichenoid tissue reaction/interface dermatitis-stomatitis, autoimmune vesiculobullous oral lesions, and immunoglobulin E- (IgE-) and immune complex-mediated oral reactions to drugs.

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