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Journal articles on the topic 'Autoimmune diseases – Animal models'

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Published: 4 June 2021
Last updated: 31 January 2023

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1

Burkhardt, H., and J. R. Kalden. "Animal models of autoimmune diseases." Rheumatology International 17, no. 3 (September 1997): 91–99. http://dx.doi.org/10.1007/s002960050015.

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2

Gregersen, J. W., S. Holmes, and L. Fugger. "Humanized animal models for autoimmune diseases." Tissue Antigens 63, no. 5 (May 2004): 383–94. http://dx.doi.org/10.1111/j.0001-2815.2004.00243.x.

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3

Ludewig, Burkhard, Rolf M. Zinkernagel, and Hans Hengartner. "Transgenic Animal Models for Virus-Induced Autoimmune Diseases." Experimental Physiology 85, no. 6 (November 2000): 653–59. http://dx.doi.org/10.1111/j.1469-445x.2000.02093.x.

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4

Rose, Noel R. "Autoimmune diseases in animal models and human patients." Pathophysiology 5 (June 1998): 261. http://dx.doi.org/10.1016/s0928-4680(98)81315-1.

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5

Taneja, Veena, and Chella S. David. "Lessons from animal models for human autoimmune diseases." Nature Immunology 2, no. 9 (September 2001): 781–84. http://dx.doi.org/10.1038/ni0901-781.

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6

Zhan, Xianbao, Fan Wang, Yan Bi, and Baoan Ji. "Animal models of gastrointestinal and liver diseases. Animal models of acute and chronic pancreatitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 311, no. 3 (September 1, 2016): G343—G355. http://dx.doi.org/10.1152/ajpgi.00372.2015.

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Animal models of pancreatitis are useful for elucidating the pathogenesis of pancreatitis and developing and testing novel interventions. In this review, we aim to summarize the most commonly used animal models, overview their pathophysiology, and discuss their strengths and limitations. We will also briefly describe common animal study procedures and refer readers to more detailed protocols in the literature. Although animal models include pigs, dogs, opossums, and other animals, we will mainly focus on rodent models because of their popularity. Autoimmune pancreatitis and genetically engineered animal models will be reviewed elsewhere.
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7

Tian, David H., Chamini J. Perera, and Gila Moalem-Taylor. "Neuropathic Pain in Animal Models of Nervous System Autoimmune Diseases." Mediators of Inflammation 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/298326.

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Neuropathic pain is a frequent chronic presentation in autoimmune diseases of the nervous system, such as multiple sclerosis (MS) and Guillain-Barre syndrome (GBS), causing significant individual disablement and suffering. Animal models of experimental autoimmune encephalomyelitis (EAE) and experimental autoimmune neuritis (EAN) mimic many aspects of MS and GBS, respectively, and are well suited to study the pathophysiology of these autoimmune diseases. However, while much attention has been devoted to curative options, research into neuropathic pain mechanisms and relief has been somewhat lacking. Recent studies have demonstrated a variety of sensory abnormalities in different EAE and EAN models, which enable investigations of behavioural changes, underlying mechanisms, and potential pharmacotherapies for neuropathic pain associated with these diseases. This review examines the symptoms, mechanisms, and clinical therapeutic options in these conditions and highlights the value of EAE and EAN animal models for the study of neuropathic pain in MS and GBS.
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8

Liu, Shou-Pei, Zhen-Hua Bian, Zhi-Bin Zhao, Jinjun Wang, Weici Zhang, Patrick S. C. Leung, Liang Li, and Zhe-Xiong Lian. "Animal Models of Autoimmune Liver Diseases: a Comprehensive Review." Clinical Reviews in Allergy & Immunology 58, no. 2 (February 19, 2020): 252–71. http://dx.doi.org/10.1007/s12016-020-08778-6.

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9

Liu, Yan, Christoph Meyer, Chengfu Xu, Honglei Weng, Claus Hellerbrand, Peter ten Dijke, and Steven Dooley. "Animal models of chronic liver diseases." American Journal of Physiology-Gastrointestinal and Liver Physiology 304, no. 5 (March 1, 2013): G449—G468. http://dx.doi.org/10.1152/ajpgi.00199.2012.

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Chronic liver diseases are frequent and potentially life threatening for humans. The underlying etiologies are diverse, ranging from viral infections, autoimmune disorders, and intoxications (including alcohol abuse) to imbalanced diets. Although at early stages of disease the liver regenerates in the absence of the insult, advanced stages cannot be healed and may require organ transplantation. A better understanding of underlying mechanisms is mandatory for the design of new drugs to be used in clinic. Therefore, rodent models are being developed to mimic human liver disease. However, no model to date can completely recapitulate the “corresponding” human disorder. Limiting factors are the time frame required in humans to establish a certain liver disease and the fact that rodents possess a distinct immune system compared with humans and have different metabolic rates affecting liver homeostasis. These features account for the difficulties in developing adequate rodent models for studying disease progression and for testing new pharmaceuticals to be translated into the clinic. Nevertheless, traditional and new promising animal models that mimic certain attributes of chronic liver diseases are established and being used to deepen our understanding in the underlying mechanisms of distinct liver diseases. This review aims at providing a comprehensive overview of recent advances in animal models recapitulating different features and etiologies of human liver diseases.
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10

Morahan, Grant, and Laurence Morel. "Genetics of autoimmune diseases in humans and in animal models." Current Opinion in Immunology 14, no. 6 (December 2002): 803–11. http://dx.doi.org/10.1016/s0952-7915(02)00401-6.

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11

Yu, Xinhua, and Frank Petersen. "A methodological review of induced animal models of autoimmune diseases." Autoimmunity Reviews 17, no. 5 (May 2018): 473–79. http://dx.doi.org/10.1016/j.autrev.2018.03.001.

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12

Zandman-Goddard, G., and Y. Shoenfeld. "Mycophenolate mofetil in animal models of autoimmune disease." Lupus 14, no. 3_suppl (March 2005): 12–16. http://dx.doi.org/10.1191/0961203305lu2112oa.

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Mycofenolate mofetil (MMF-Cellcept) is an immunomodulatory drug utilized extensively in transplant medicine. The efficacy of regimes including Cellcept in preventing allograft rejection, and in the treatment of rejection, is now firmly established. The immunosuppressive actions of this drug enabled the investigation for the beneficial effects in autoimmune diseases. We review the evidence for the contribution of MMF in autoimmunity in animal models of systemic lupus erythematosus (SLE), mercury induced autoimmune glomerulonephritis, diabetes mellitus, experimental autoimmune uveoretinitis, and experimental allergic encephalitis. MMF has an influence on the T and B cell pathways. It is immunosuppressive and anti-inflammatory.
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13

Lin, Mei, Zuomin Wang, and Xiaozhe Han. "B Cells with Regulatory Function in Animal Models of Autoimmune and Non-Autoimmune Diseases." Open Journal of Immunology 05, no. 01 (2015): 9–17. http://dx.doi.org/10.4236/oji.2015.51002.

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14

Lee, Byung Ha, Adrienne E. Gauna, Kaleb M. Pauley, Yun-Jong Park, and Seunghee Cha. "Animal Models in Autoimmune Diseases: Lessons Learned from Mouse Models for Sjögren’s Syndrome." Clinical Reviews in Allergy & Immunology 42, no. 1 (November 22, 2011): 35–44. http://dx.doi.org/10.1007/s12016-011-8288-5.

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15

Burkhardt, H., and J. R. Kalden. "Xenobiotic immunosuppressive agents: therapeutic effects in animal models of autoimmune diseases." Rheumatology International 17, no. 3 (September 1997): 85–90. http://dx.doi.org/10.1007/s002960050014.

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16

Trzos, Katarzyna, Natalia Pydyn, Jolanta Jura, and Jerzy Kotlinowski. "Selected transgenic murine models of human autoimmune liver diseases." Pharmacological Reports 74, no. 2 (January 15, 2022): 263–72. http://dx.doi.org/10.1007/s43440-021-00351-y.

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AbstractMurine models of human diseases are of outmost importance for both studying molecular mechanisms driving their development and testing new treatment strategies. In this review, we first discuss the etiology and risk factors for autoimmune liver disease, including primary biliary cholangitis, autoimmune hepatitis and primary sclerosing cholangitis. Second, we highlight important features of murine transgenic models that make them useful for basic scientists, drug developers and clinical researchers. Next, a brief description of each disease is followed by the characterization of selected animal models.
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17

Ghareghani, Majid, Amir Ghanbari, Ali Eid, Abdullah Shaito, Wael Mohamed, Stefania Mondello, and Kazem Zibara. "Hormones in experimental autoimmune encephalomyelitis (EAE) animal models." Translational Neuroscience 12, no. 1 (January 1, 2021): 164–89. http://dx.doi.org/10.1515/tnsci-2020-0169.

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Abstract Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) in which activated immune cells attack the CNS and cause inflammation and demyelination. While the etiology of MS is still largely unknown, the interaction between hormones and the immune system plays a role in disease progression, but the mechanisms by which this occurs are incompletely understood. Several in vitro and in vivo experimental, but also clinical studies, have addressed the possible role of the endocrine system in susceptibility and severity of autoimmune diseases. Although there are several demyelinating models, experimental autoimmune encephalomyelitis (EAE) is the oldest and most commonly used model for MS in laboratory animals which enables researchers to translate their findings from EAE into human. Evidences imply that there is great heterogeneity in the susceptibility to the induction, the method of induction, and the response to various immunological or pharmacological interventions, which led to conflicting results on the role of specific hormones in the EAE model. In this review, we address the role of endocrine system in EAE model to provide a comprehensive view and a better understanding of the interactions between the endocrine and the immune systems in various models of EAE, to open up a ground for further detailed studies in this field by considering and comparing the results and models used in previous studies.
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18

SCHORLEMMER, HANS-ULRICH, and GERHARD DICKNEITE. "Preclinical Studies with 15-Deoxyspergualin in Various Animal Models for Autoimmune Diseases." Annals of the New York Academy of Sciences 685, no. 1 Immunomodulat (June 1993): 155–74. http://dx.doi.org/10.1111/j.1749-6632.1993.tb35862.x.

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19

Watanabe, Norihiko, and Hiroshi Nakajima. "Coinhibitory Molecules in Autoimmune Diseases." Clinical and Developmental Immunology 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/269756.

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Coinhibitory molecules such as CTLA-4, PD-1 and BTLA negatively regulate immune responses. Multiple studies indicate that the deficiency or mutation of coinhibitory molecules leads to the development of autoimmune diseases in mice and humans, indicating that the negative signals from coinhibitory molecules are crucial for the prevention of autoimmunity. In some conditions, the administration of decoy coinhibitory receptors (e.g., CTLA-4 Ig) or mAb against coinhibitory molecules suppresses the responses of self-reactive T cells in autoimmune diseases. Therefore, modulation of coinhibitory signals seems to be an attractive approach to induce tolerance in autoimmune diseases in humans where the disease-inducing self-antigens are not known. Particularly, administration of CTLA-4 Ig has shown great promise in animal models of autoimmune diseases and has been gaining increasing attention in clinical investigation in several autoimmune diseases in humans.
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20

Kunz, Manfred, and Saleh M. Ibrahim. "Cytokines and Cytokine Profiles in Human Autoimmune Diseases and Animal Models of Autoimmunity." Mediators of Inflammation 2009 (2009): 1–20. http://dx.doi.org/10.1155/2009/979258.

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The precise pathomechanisms of human autoimmune diseases are still poorly understood. However, a deepened understanding of these is urgently needed to improve disease prevention and early detection and guide more specific treatment approaches. In recent years, many new genes and signalling pathways involved in autoimmunity with often overlapping patterns between different disease entities have been detected. Major contributions were made by experiments using DNA microarray technology, which has been used for the analysis of gene expression patterns in chronic inflammatory and autoimmune diseases, among which were rheumatoid arthritis, systemic lupus erythematosus, psoriasis, systemic sclerosis, multiple sclerosis, and type-1 diabetes. In systemic lupus erythematosus, a so-called interferon signature has been identified. In psoriasis, researchers found a particular immune signalling cluster. Moreover the identification of a new subset of inflammatory T cells, so-called Th17 T cells, secreting interleukin (IL)-17 as one of their major cytokines and the identification of the IL-23/IL-17 axis of inflammation regulation, have significantly improved our understanding of autoimmune diseases. Since a plethora of new treatment approaches using antibodies or small molecule inhibitors specifically targeting cytokines, cellular receptors, or signalling mechanisms has emerged in recent years, more individualized treatment for affected patients may be within reach in the future.
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21

Hashida, Ryoichi, Yasunori Shimozuru, Jessica Chang, Ibis Agosto-Marlin, Takaki Waritani, and Kuniaki Terato. "New Studies of Pathogenesis of Rheumatoid Arthritis with Collagen-Induced and Collagen Antibody-Induced Arthritis Models: New Insight Involving Bacteria Flora." Autoimmune Diseases 2021 (March 25, 2021): 1–13. http://dx.doi.org/10.1155/2021/7385106.

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Much public research suggests that autoimmune diseases such as rheumatoid arthritis (RA) are induced by aberrant “self” immune responses attacking autologous tissues and organ components. However, recent studies have reported that autoimmune diseases may be triggered by dysbiotic composition changes of the intestinal bacteria and an imbalance between these bacteria and intestinal immune systems. However, there are a few solid concepts or methods to study the putative involvement and relationship of these inner environmental factors in RA pathogenesis. Fortunately, Collagen-Induced Arthritis (CIA) and Collagen Antibody-Induced Arthritis (CAIA) models have been widely used as animal models for studying the pathogenesis of RA. In addition to RA, these models can be extensively used as animal models for studying complicated hypotheses in many diseases. In this review, we introduce some basic information about the CIA and CAIA models as well as how to apply these models effectively to investigate relationships between the pathogenesis of autoimmune diseases, especially RA, and the dysbiosis of intestinal bacterial flora.
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22

Blumenstein, Irina. "Intestinale Dysbiose und Mikrobiomtransfer bei Autoimmunerkrankungen." Kompass Autoimmun 3, no. 2 (2021): 73–74. http://dx.doi.org/10.1159/000515923.

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Recent studies have shown that a number of common autoimmune diseases have perturbations of their intestinal microbiome (dysbiosis). These include: Celiac Disease (CeD), Multiple Sclerosis (MS), Rheumatoid Arthritis (RA), Sjogren’s Syndrome (SS), and Type 1 diabetes (T1D). All of these have intestinal microbiomes that are different from healthy controls. There have been numerous studies using animal models of single probiotics (monoclonal) or mixtures of probiotics (polyclonal) and even complete microbiota transfer (fecal microbial transfer-FMT) to inhibit or delay the onset of autoimmune diseases such as the aforementioned common ones. However, proportionally, fewer clinical trials have utilized monoclonal therapies or FMT than polyclonal therapies for treating autoimmune diseases, even though bacterial mono-therapies do inhibit the development of autoimmune diseases and/or delay the onset of autoimmune diseases in rodent models of those autoimmune diseases. In this review then, we review the previously completed and currently ongoing clinical trials that are testing bacterial therapies (FMT, monoclonal, and polyclonal) to treat common autoimmune diseases and discuss the successes in using bacterial monotherapies to treat rodent models of these common autoimmune diseases.
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23

Fan, Xueli, Hongliang Zhang, Yun Cheng, Xinmei Jiang, Jie Zhu, and Tao Jin. "Double Roles of Macrophages in Human Neuroimmune Diseases and Their Animal Models." Mediators of Inflammation 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/8489251.

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Macrophages are important immune cells of the innate immune system that are involved in organ-specific homeostasis and contribute to both pathology and resolution of diseases including infections, cancer, obesity, atherosclerosis, and autoimmune disorders. Multiple lines of evidence point to macrophages as a remarkably heterogeneous cell type. Different phenotypes of macrophages exert either proinflammatory or anti-inflammatory roles depending on the cytokines and other mediators that they are exposed to in the local microenvironment. Proinflammatory macrophages secrete detrimental molecules to induce disease development, while anti-inflammatory macrophages produce beneficial mediators to promote disease recovery. The conversion of the phenotypes of macrophages can regulate the initiation, development, and recovery of autoimmune diseases. Human neuroimmune diseases majorly include multiple sclerosis (MS), neuromyelitis optica (NMO), myasthenia gravis (MG), and Guillain-Barré syndrome (GBS) and macrophages contribute to the pathogenesis of these neuroimmune diseases. In this review, we summarize the double roles of macrophage in neuroimmune diseases and their animal models to further explore the mechanisms of macrophages involved in the pathogenesis of these disorders, which may provide a potential therapeutic approach for these disorders in the future.
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24

Das, Pranab K., and Graham Elliott. "Conference Scene: Lessons from animal models of autoimmune diseases: from mechanisms to applications." Immunotherapy 3, no. 2 (February 2011): 147–51. http://dx.doi.org/10.2217/imt.10.102.

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25

Leung, Patrick S. C., Shang-An Shu, Thomas P. Kenny, Ping-Yi Wu, and Mi-Hua Tao. "Development and validation of gene therapies in autoimmune diseases: Epidemiology to animal models." Autoimmunity Reviews 9, no. 5 (March 2010): A400—A405. http://dx.doi.org/10.1016/j.autrev.2009.12.009.

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26

Stimmer, Lev, Claire-Maëlle Fovet, and Ché Serguera. "Experimental Models of Autoimmune Demyelinating Diseases in Nonhuman Primates." Veterinary Pathology 55, no. 1 (June 6, 2017): 27–41. http://dx.doi.org/10.1177/0300985817712794.

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Human idiopathic inflammatory demyelinating diseases (IIDD) are a heterogeneous group of autoimmune inflammatory and demyelinating disorders of the central nervous system (CNS). These include multiple sclerosis (MS), the most common chronic IIDD, but also rarer disorders such as acute disseminated encephalomyelitis (ADEM) and neuromyelitis optica (NMO). Great efforts have been made to understand the pathophysiology of MS, leading to the development of a few effective treatments. Nonetheless, IIDD still require a better understanding of the causes and underlying mechanisms to implement more effective therapies and diagnostic methods. Experimental autoimmune encephalomyelitis (EAE) is a commonly used animal model to study the pathophysiology of IIDD. EAE is principally induced through immunization with myelin antigens combined with immune-activating adjuvants. Nonhuman primates (NHP), the phylogenetically closest relatives of humans, challenged by similar microorganisms as other primates may recapitulate comparable immune responses to that of humans. In this review, the authors describe EAE models in 3 NHP species: rhesus macaques ( Macaca mulatta), cynomolgus macaques ( Macaca fascicularis), and common marmosets ( Callithrix jacchus), evaluating their respective contribution to the understanding of human IIDD. EAE in NHP is a heterogeneous disease, including acute monophasic and chronic polyphasic forms. This diversity makes it a versatile model to use in translational research. This clinical variability also creates an opportunity to explore multiple facets of immune-mediated mechanisms of neuro-inflammation and demyelination as well as intrinsic protective mechanisms. Here, the authors review current insights into the pathogenesis and immunopathological mechanisms implicated in the development of EAE in NHP.
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27

Delogu, Lucia Gemma, Silvia Deidda, Giuseppe Delitala, and Roberto Manetti. "Infectious diseases and autoimmunity." Journal of Infection in Developing Countries 5, no. 10 (October 11, 2011): 679–87. http://dx.doi.org/10.3855/jidc.2061.

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Introduction: Autoimmunity occurs when the immune system recognizes and attacks host tissue. In addition to genetic factors, environmental triggers (in particular viruses, bacteria and other infectious pathogens) are thought to play a major role in the development of autoimmune diseases. Methodology: We searched PubMed, Cochrane, and Scopus without time limits for relevant articles. Results: In this review, we (i) describe the ways in which an infectious agent can initiate or exacerbate autoimmunity; (ii) discuss the evidence linking certain infectious agents to autoimmune diseases in humans; and (iii) describe the animal models used to study the link between infection and autoimmunity. Conclusions: Besides genetic predisposition to autoimmunity, viral and bacterial infections are known to be involved in the initiation and promotion of autoimmune diseases. These studies suggest that pathogens can trigger autoimmunity through molecular mimicry and their adjuvant effects during initiation of disease, and can promote autoimmune responses through bystander activation or epitope spreading via inflammation and/or superantigens.
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28

WICK, GEORG, ROSWITHA SGONC, and OSKAR LECHNER. "Neuroendocrine-Immune Disturbances in Animal Models with Spontaneous Autoimmune Diseasesa." Annals of the New York Academy of Sciences 840, no. 1 (May 1998): 591–98. http://dx.doi.org/10.1111/j.1749-6632.1998.tb09598.x.

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29

Park, Tae-Yoon, and Kwang-Soo Kim. "Chloroquine modulates inflammatory autoimmune responses through Nurr1 in autoimmune diseases." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 238.9. http://dx.doi.org/10.4049/jimmunol.204.supp.238.9.

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Abstract For over a half-century the anti-malarial drug chloroquine (CQ) has been used as a therapeutic agent, alone or in combination, to treat autoimmune diseases. However, neither the underlying mechanism(s) of action nor their molecular target(s) are well defined. The orphan nuclear receptor Nurr1 (also known as NR4A2) is an essential transcription factor affecting the development and maintenance of midbrain dopaminergic neurons. In this study, using in vitro T cell differentiation models, we demonstrate that CQ activates TREG cell differentiation and induces Foxp3 gene expression in a Nurr1-dependent manner. Remarkably, CQ appears to induce Nurr1 function by two distinct mechanisms: firstly, by direct binding to Nurr1’s ligand-binding domain and promoting its transcriptional activity and secondly by upregulation of Nurr1 expression through the CREB signaling pathway. In contrast, CQ suppressed gene expression and differentiation of pathogenic TH17 cells. Importantly, using a valid animal model of inflammatory bowel disease (IBD), we demonstrated that CQ promotes Foxp3 expression and differentiation of TREG cells in a Nurr1-dependent manner, leading to significant improvement of IBD-related symptoms. Taken together, these data suggest that CQ ameliorates autoimmune diseases via regulating Nurr1 function/expression and that Nurr1 is a promising target for developing effective therapeutics of human inflammatory autoimmune diseases.
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30

Hultqvist, M., K. S. Nandakumar, U. Björklund, and R. Holmdahl. "The novel small molecule drug Rabeximod is effective in reducing disease severity of mouse models of autoimmune disorders." Annals of the Rheumatic Diseases 68, no. 1 (March 17, 2008): 130–35. http://dx.doi.org/10.1136/ard.2007.085241.

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Objectives:Autoimmune diseases such as rheumatoid arthritis (RA) and multiple sclerosis (MS) affect a relatively large portion of the population, leading to severe disability if left untreated. Even though pharmaceutics targeting the immune system have revolutionised the therapy of these diseases, there is still a need for novel, more effective therapeutic substances. One such substance is the new chemical entity 9-chloro-2,3 dimethyl-6-(N,N-dimthylamino-2-oxoethyl)-6H-indolo [2,3-b] quionoxaline, Rabeximod, currently being investigated for efficiency in treatment of human RA. In this study we aimed to evaluate Rabeximod as a treatment for autoimmune diseases, using animal models.Methods:In the present investigation we have evaluated Rabeximod as a treatment for autoimmune diseases using mouse models of RA and MS, ie, collagen-induced arthritis, collagen antibody induced arthritis and experimental autoimmune encephalomyelitis.Results:Rabeximod efficiently prevented arthritis and encephalomyelitis in mice. In addition, this effect correlated to the timepoint when cells migrate into the joints.Conclusions:We conclude that Rabeximod reduces disease severity in animal models of autoimmunity and should be considered as a new therapeutic substance for MS and RA.
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Lee, Hong Kyung, Sang Hee Lim, In Sung Chung, Yunsoo Park, Mi Jeong Park, Ju Young Kim, Yong Guk Kim, Jin Tae Hong, Youngsoo Kim, and Sang-Bae Han. "Preclinical Efficacy and Mechanisms of Mesenchymal Stem Cells in Animal Models of Autoimmune Diseases." Immune Network 14, no. 2 (2014): 81. http://dx.doi.org/10.4110/in.2014.14.2.81.

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32

CARLSON, RICHARD P., WILLIAM L. BAEDER, ROBERT G. CACCESE, LINDA M. WARNER, and SUREN N. SEHGAL. "Effects of Orally Administered Rapamycin in Animal Models of Arthritis and Other Autoimmune Diseases." Annals of the New York Academy of Sciences 685, no. 1 Immunomodulat (June 1993): 86–113. http://dx.doi.org/10.1111/j.1749-6632.1993.tb35855.x.

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33

Wu, Dayong. "Green tea EGCG, T-cell function, and T-cell-mediated autoimmune encephalomyelitis." Journal of Investigative Medicine 64, no. 8 (August 16, 2016): 1213–19. http://dx.doi.org/10.1136/jim-2016-000158.

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Autoimmune diseases are common, disabling immune disorders affecting millions of people. Recent studies indicate that dysregulated balance of different CD4+T-cell subpopulations plays a key role in immune pathogenesis of several major autoimmune diseases. Green tea and its active ingredient, epigallocatechin-3-gallate (EGCG), have been shown to modulate immune cell functions and improve some autoimmune diseases in animal models. In a series of studies we determined EGCG's effect on T-cell functions and its application in autoimmune diseases. We first observed that EGCG inhibited CD4+T-cell expansion induced by polyclonal (mitogens or anti-CD3/CD28) or antigen-specific stimulation. We then showed that EGCG suppressed expansion and cell cycle progression of naïve CD4+T by modulating cell cycle-related proteins. EGCG also inhibited naive CD4+T-cell differentiation into Th1 and Th17 effector subsets by impacting their respective signaling transducers and transcription factors. These results suggest that EGCG may improve T-cell-mediated autoimmune diseases. Using the experimental autoimmune encephalomyelitis (EAE) mice, an animal model for human multiple sclerosis, we found that dietary supplementation with EGCG attenuated the disease's symptoms and pathology. These EGCG-induced changes are associated with findings in the immune and inflammation profiles in lymphoid tissues and the central nervous system: a reduction in proliferation of autoreactive T cells, production of proinflammatory cytokines, and Th1 and Th17 subpopulations, and an increase in regulatory T-cell populations. These results suggest that green tea or its active components may have a preventive and therapeutic potential in dealing with T-cell-mediated autoimmune diseases. However, the translational value of these findings needs to be validated in future human studies.
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Lee, Min Ho, Jae Il Shin, Jae Won Yang, Keum Hwa Lee, Do Hyeon Cha, Jun Beom Hong, Yeoeun Park, et al. "Genome Editing Using CRISPR-Cas9 and Autoimmune Diseases: A Comprehensive Review." International Journal of Molecular Sciences 23, no. 3 (January 25, 2022): 1337. http://dx.doi.org/10.3390/ijms23031337.

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Autoimmune diseases are disorders that destruct or disrupt the body’s own tissues by its own immune system. Several studies have revealed that polymorphisms of multiple genes are involved in autoimmune diseases. Meanwhile, gene therapy has become a promising approach in autoimmune diseases, and clustered regularly interspaced palindromic repeats and CRISPR-associated protein 9 (CRISPR-Cas9) has become one of the most prominent methods. It has been shown that CRISPR-Cas9 can be applied to knock out proprotein convertase subtilisin/kexin type 9 (PCSK9) or block PCSK9, resulting in lowering low-density lipoprotein cholesterol. In other studies, it can be used to treat rare diseases such as ornithine transcarbamylase (OTC) deficiency and hereditary tyrosinemia. However, few studies on the treatment of autoimmune disease using CRISPR-Cas9 have been reported so far. In this review, we highlight the current and potential use of CRISPR-Cas9 in the management of autoimmune diseases. We summarize the potential target genes for immunomodulation using CRISPR-Cas9 in autoimmune diseases including rheumatoid arthritis (RA), inflammatory bowel diseases (IBD), systemic lupus erythematosus (SLE), multiple sclerosis (MS), type 1 diabetes mellitus (DM), psoriasis, and type 1 coeliac disease. This article will give a new perspective on understanding the use of CRISPR-Cas9 in autoimmune diseases not only through animal models but also in human models. Emerging approaches to investigate the potential target genes for CRISPR-Cas9 treatment may be promising for the tailored immunomodulation of some autoimmune diseases in the near future.
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Zampieri, Roberta, Annalisa Brozzetti, Eva Pericolini, Elena Bartoloni, Elena Gabrielli, Elena Roselletti, George Lomonosoff, et al. "Prevention and treatment of autoimmune diseases with plant virus nanoparticles." Science Advances 6, no. 19 (May 2020): eaaz0295. http://dx.doi.org/10.1126/sciadv.aaz0295.

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Plant viruses are natural, self-assembling nanostructures with versatile and genetically programmable shells, making them useful in diverse applications ranging from the development of new materials to diagnostics and therapeutics. Here, we describe the design and synthesis of plant virus nanoparticles displaying peptides associated with two different autoimmune diseases. Using animal models, we show that the recombinant nanoparticles can prevent autoimmune diabetes and ameliorate rheumatoid arthritis. In both cases, this effect is based on a strictly peptide-related mechanism in which the virus nanoparticle acts both as a peptide scaffold and as an adjuvant, showing an overlapping mechanism of action. This successful preclinical testing could pave the way for the development of plant viruses for the clinical treatment of human autoimmune diseases.
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36

Klinker, Matthew W. "Mesenchymal stem cells in the treatment of inflammatory and autoimmune diseases in experimental animal models." World Journal of Stem Cells 7, no. 3 (2015): 556. http://dx.doi.org/10.4252/wjsc.v7.i3.556.

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37

Di Niro, Roberto, Federica Ziller, Fiorella Florian, Sergio Crovella, Marco Stebel, Marco Bestagno, Oscar Burrone, et al. "Construction of miniantibodies for the in vivo study of human autoimmune diseases in animal models." BMC Biotechnology 7, no. 1 (2007): 46. http://dx.doi.org/10.1186/1472-6750-7-46.

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38

Hollenbach, Stanley J., Greg Coffey, Francis R. DeGuzman, Mayuko Inagaki, Anjali Pandey, Zhaozhong J. Jia, Qing Xu, et al. "Inhibition of Syk Activity Is Sufficient for Inhibitory Effect in Animal Models of Autoimmune Diseases." Blood 112, no. 11 (November 16, 2008): 680. http://dx.doi.org/10.1182/blood.v112.11.680.680.

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Abstract Spleen tyrosine kinase (Syk) serves as a key mediator of Fc receptor-mediated signaling in immunologic signaling cascades. Human Phase II trials have reported that dual inhibition of Syk and Janus kinases (JAK) by agents such as R788 (tamatinib fosdium) result in clinical benefit in rheumatoid arthritis (RA) and idiopathic thrombocytopenia purpura (ITP) patients. In order to delineate if inhibition of Syk alone was sufficient to produce a treatment benefit, we utilized compounds from two chemically diverse series of oral Syk inhibitors with differing kinase specificity in mouse models of RA and ITP. Compounds from the first series (P142–76, P459–72) were potent inhibitors of purified Syk (IC50 = 4 to 43nM) and when tested at a ten fold higher concentration (300–500nM), lacked JAK inhibitory activity. Even at a concentration of 5μM, P142–76 did not inhibit JAK activity. Compounds from the second series (P420–1, P420–89) were potent Syk inhibitors (IC50 = 15 to 31nM) and also exhibited comparable inhibitory potency against purified JAK (IC50 JAK1 = 6–7nM, JAK2 = 2–3nM, JAK3 = 0.6–0.8nM). The compounds inhibited B cell receptor-induced activation of primary mouse splenocytes; P420–89 (IC50 ~ 50nM) being somewhat more potent than P459–72 (IC50 = 125–250nM). Importantly, phorbol 12-myristate 13-acetate (PMA)-induced B cell activation was not inhibited by any of the compounds at the tested concentration (1μM). Further, oral dosing of these compounds inhibited B cell receptor-induced B cell activation in mice. The RA model (n=12/group) investigated collagen antibody induced arthritis over a seven to ten day time course. The ITP model (n=10/group) utilized rapid clearance and destruction of antibody-coated platelets by phagocytic cells such as spleen macrophages. In this model, mice injected with a rat anti-mouse CD41 antibody became thrombocytopenic (average of 49% reduction in number of circulating platelets) over the 8h time course of experimentation. Model Kinase specificity Agent, Dose per day Average peak plasma concentration (μM) Average inhibitory activity (%) * denotes statistically significant reduction (p<0.05) in inflammation score (RA) or platelet clearance (ITP) compared to vehicle by two-tailed, unpaired Student’s t test. RA Syk P459–72, 100mg/kg 10.2 88* RA Syk P459–72, 30mg/kg 4.4 27* RA Syk/JAK P420–89, 30mg/kg 6.9 57* RA Syk/JAK P420–89, 10mg/kg 0.8 0 ITP Syk P142–76, 30mg/kg 2.1 82* ITP Syk/JAK P420–1, 10mg/kg 2.8 50* ITP Syk/JAK P420–1, 3mg/kg 0.4 17* ITP Syk/JAK P420–89, 30mg/kg 5.4 44* ITP Syk/JAK P420–89, 10mg/kg 0.6 4 In the RA studies, in addition to macroscopic signs of arthritis and assessment of clinical score, positive results were also verified histologically by reductions in peri-articular edema and neutrophil count and by scoring of intra-articular neutrophils and fibrin. In the ITP studies, mice pre-treated with P142–76, P420–1 or P420–89 were protected from loss of platelets, while mice pre-treated with vehicle alone displayed no protection. Our results highlight the role of Syk inhibition by small molecule oral inhibitors and suggest that inhibition of Syk activity, without dual inhibition of Syk/JAK, may be a promising strategy for therapeutic intervention in human autoimmune and inflammatory diseases.
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39

Yeste, Ada, and Francisco J. Quintana. "Antigen Microarrays for the Study of Autoimmune Diseases." Clinical Chemistry 59, no. 7 (July 1, 2013): 1036–44. http://dx.doi.org/10.1373/clinchem.2012.194423.

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BACKGROUND The immune response involves the activation of heterogeneous populations of T cells and B cells that show different degrees of affinity and specificity for target antigens. Although several techniques have been developed to study the molecular pathways that control immunity, there is a need for high-throughput assays to monitor the specificity of the immune response. CONTENT Antigen microarrays provide a new tool to study the immune response. We reviewed the literature on antigen microarrays and their advantages and limitations, and we evaluated their use for the study of autoimmune diseases. Antigen arrays have been successfully used for several purposes in the investigation of autoimmune disorders: for disease diagnosis, to monitor disease progression and response to therapy, to discover mechanisms of pathogenesis, and to tailor antigen-specific therapies to the autoimmune response of individual patients. In this review we discuss the use of antigen microarrays for the study of 4 common autoimmune diseases and their animal models: type 1 diabetes, systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis. CONCLUSIONS Antigen microarrays constitute a new tool for the investigation of the immune response in autoimmune disorders and also in other conditions such as tumors and allergies. Once current limitations are overcome, antigen microarrays have the potential to revolutionize the investigation and management of autoimmune diseases.
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40

Corneth, Odilia B. J., Stefan F. H. Neys, and Rudi W. Hendriks. "Aberrant B Cell Signaling in Autoimmune Diseases." Cells 11, no. 21 (October 27, 2022): 3391. http://dx.doi.org/10.3390/cells11213391.

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Aberrant B cell signaling plays a critical in role in various systemic and organ-specific autoimmune diseases. This is supported by genetic evidence by many functional studies in B cells from patients or specific animal models and by the observed efficacy of small-molecule inhibitors. In this review, we first discuss key signal transduction pathways downstream of the B cell receptor (BCR) that ensure that autoreactive B cells are removed from the repertoire or functionally silenced. We provide an overview of aberrant BCR signaling that is associated with inappropriate B cell repertoire selection and activation or survival of peripheral B cell populations and plasma cells, finally leading to autoantibody formation. Next to BCR signaling, abnormalities in other signal transduction pathways have been implicated in autoimmune disease. These include reduced activity of several phosphates that are downstream of co-inhibitory receptors on B cells and increased levels of BAFF and APRIL, which support survival of B cells and plasma cells. Importantly, pathogenic synergy of the BCR and Toll-like receptors (TLR), which can be activated by endogenous ligands, such as self-nucleic acids, has been shown to enhance autoimmunity. Finally, we will briefly discuss therapeutic strategies for autoimmune disease based on interfering with signal transduction in B cells.
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41

Zhong, Yajie, Xuan Zhang, and Waipo Chong. "Interleukin-24 Immunobiology and Its Roles in Inflammatory Diseases." International Journal of Molecular Sciences 23, no. 2 (January 6, 2022): 627. http://dx.doi.org/10.3390/ijms23020627.

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Interleukin (IL)-24 belongs to the IL-10 family and signals through two receptor complexes, i.e., IL-20RA/IL-20RB and IL-20RB/IL22RA1. It is a multifunctional cytokine that can regulate immune response, tissue homeostasis, host defense, and oncogenesis. Elevation of IL-24 is associated with chronic inflammation and autoimmune diseases, such as psoriasis, rheumatoid arthritis (RA), and inflammatory bowel disease (IBD). Its pathogenicity has been confirmed by inducing inflammation and immune cell infiltration for tissue damage. However, recent studies also revealed their suppressive functions in regulating immune cells, including T cells, B cells, natural killer (NK) cells, and macrophages. The tolerogenic properties of IL-24 were reported in various animal models of autoimmune diseases, suggesting the complex functions of IL-24 in regulating autoimmunity. In this review, we discuss the immunoregulatory functions of IL-24 and its roles in autoimmune diseases.
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Seder, R. A., B. L. Kelsall, and D. Jankovic. "Differential roles for IL-12 in the maintenance of immune responses in infectious versus autoimmune disease." Journal of Immunology 157, no. 7 (October 1, 1996): 2745–48. http://dx.doi.org/10.4049/jimmunol.157.7.2745.

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Abstract IL-12 has been shown to be important in the generation of a functional Th1 response in animal models of both infectious and autoimmune disease. Furthermore, the role of IL-12 in the maintenance of the immune responses in these diseases is now emerging. Herein, we discuss the idea that memory responses for certain infections may be IL-12 independent, whereas memory responses for specific autoimmune diseases still require IL-12 to maintain a pathogenic response.
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43

Farak Gomez, Juan. "Immunomodulation by helmintos: Possible use as therapy for autoimmune diseases." MOJ Biology and Medicine 6, no. 2 (2021): 97–99. http://dx.doi.org/10.15406/mojbm.2021.06.00139.

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Context: The incidence of autoimmune diseases and allergies has increased markedly in the last half of the 20th century, especially in more developed countries, with an increase in urbanization and hygiene that has led to the elimination of many parasitic infections. Objective: To analyze through scientific bibliographic sources the effects of the parasite load, especially helminthiasis, on the appearance of autoimmune and allergic diseases. Methodology: The documentary analysis of different scientific sources that refer to the theory of immunomodulation by helminths was used. Results: They suggest that the treatment of autoimmune diseases with helminths or products derived from them can have protective and therapeutic effects in these patients. Conclusions: It could be concluded that the immunodulation mechanisms carried out by helminths prevent patients from eliminating the parasites, but have beneficial effects on the course of some autoimmune diseases. Although the causal relationship is not fully proven, studies in animal models and clinical trials carried out in patients with autoimmune diseases suggest that their treatment with helminths or products derived from them may have protective and therapeutic effects in these patients.
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44

Okorogu, Rita, Prasanth Surampudi, Isela Valera, Ramesh Halder, Chetachi Okereke, Christina Wang, Ronald Swerdloff, and Ram Singh. "Increased autoimmunity in men with Klinefelter’s syndrome: Sex chromosome dosage effect (P3309)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 175.2. http://dx.doi.org/10.4049/jimmunol.190.supp.175.2.

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Abstract Autoimmune diseases are more common in women than in men. Studies in animal models suggest a role of sex chromosome genotype in modulating autoimmune susceptibility. Here, we begin to translate these murine findings onto humans. Our hypothesis is that X chromosome dosage, rather than the female sex itself, imparts susceptibility to autoimmune diseases. Our results show that levels of IgG anti-chromatin and anti-nucleosome autoantibodies were significantly higher in men with sex chromosome aneuploidy (47,XXY) compared to 46,XY men. XXY men, however, did not have non-specific B cell hyper-reactivity, as the levels of anti-thyroid peroxidase antibody that is associated with autoimmune thyroid disease were similar between the two groups. A preliminary analysis of completed questionnaire revealed an increase in autoimmune and inflammatory conditions when compared with known population prevalence of these diseases. Analysis of immune cell phenotype and responses conducted thus far showed a significant reduction in the frequency of natural killer T cells in 47,XXY men as compared to 46,XY men. These data suggest a role of X chromosome dosage in inducing autoimmunity in humans. Since animals and humans with autoimmune diseases have reduced numbers and/or functions of natural killer T cells, our observation of reduced natural killer T cells in 47,XXY men may be related to increased autoimmunity in these men.
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45

Wilkinson, S. E., and J. S. Nixon. "PKC Inhibitors in the Therapy of Autoimmune Diseases." Current Pharmaceutical Design 2, no. 6 (December 1996): 596–609. http://dx.doi.org/10.2174/1381612802666221004184418.

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The protein kinase C ( PKC) family of isoenzymes was thought to mediate a wide range of signal transduction processes in cells. However, it is now widely accepted that its role may have been overstated. The advent of selective PKC inhibitors has led to a re-appraisal of the role this enzyme plays in these processes. This review shows how the structural lead provided by staurosporine, a non-selective protein kinase inhibitor, was used as a basis for the design of substituted bisindolylmaleimides with significantly improved selectivity for protein kinase C over cAMP-dependent protein kinase and phophorylase kinase. Evidence from studies with these inhibitors implicates PKC in inflammatory responses such as the neutrophil respiratory burst and antigen-driven T cell proliferation. Potent, orally bioavailable bisindolylmaleimide PKC inhibito_rs such as Ro 32-0432 inhibit phorbol ester -induced inflammation in rodents. These agents also selectively inhibit T cell mediated responses in animal models of arthritis and encephalomyelitis. Taken together, these results suggest that selective inhibitors of PKC may be useful in the therapy of autoimmune diseases such as rheumatoid arthritis, multiple sclerosis and psoriasis.
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46

Ma, Huijuan, and Chang-Qing Xia. "Phenotypic and Functional Diversities of Myeloid-Derived Suppressor Cells in Autoimmune Diseases." Mediators of Inflammation 2018 (December 23, 2018): 1–8. http://dx.doi.org/10.1155/2018/4316584.

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Myeloid-derived suppressor cells (MDSCs) are identified as a heterogeneous population of cells with the function to suppress innate as well as adaptive immune responses. The initial studies of MDSCs were primarily focused on the field of animal tumor models or cancer patients. In cancer, MDSCs play the deleterious role to inhibit tumor immunity and to promote tumor development. Over the past few years, an increasing number of studies have investigated the role of MDSCs in autoimmune diseases. The beneficial effects of MDSCs in autoimmunity have been reported by some studies, and thus, immunosuppressive MDSCs may be a novel therapeutic target in autoimmune diseases. There are some controversial findings as well. Many questions such as the activation, differentiation, and suppressive functions of MDSCs and their roles in autoimmune diseases remain unclear. In this review, we have discussed the current understanding of MDSCs in autoimmune diseases.
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47

Rotondi, Mario, Luca Chiovato, Sergio Romagnani, Mario Serio, and Paola Romagnani. "Role of Chemokines in Endocrine Autoimmune Diseases." Endocrine Reviews 28, no. 5 (August 1, 2007): 492–520. http://dx.doi.org/10.1210/er.2006-0044.

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Chemokines are a group of peptides of low molecular weight that induce the chemotaxis of different leukocyte subtypes. The major function of chemokines is the recruitment of leukocytes to inflammation sites, but they also play a role in tumoral growth, angiogenesis, and organ sclerosis. In the last few years, experimental evidence accumulated supporting the concept that interferon-γ (IFN-γ) inducible chemokines (CXCL9, CXCL10, and CXCL11) and their receptor, CXCR3, play an important role in the initial stage of autoimmune disorders involving endocrine glands. The fact that, after IFN-γ stimulation, endocrine epithelial cells secrete CXCL10, which in turn recruits type 1 T helper lymphocytes expressing CXCR3 and secreting IFN-γ, thus perpetuating autoimmune inflammation, strongly supports the concept that chemokines play an important role in endocrine autoimmunity. This article reviews the recent literature including basic science, animal models, and clinical studies, regarding the role of these chemokines in autoimmune endocrine diseases. The potential clinical applications of assaying the serum levels of CXCL10 and the value of such measurements are reviewed. Clinical studies addressing the issue of a role for serum CXCL10 measurement in Graves’ disease, Graves’ ophthalmopathy, chronic autoimmune thyroiditis, type 1 diabetes mellitus, and Addison’s disease have been considered. The principal aim was to propose that chemokines, and in particular CXCL10, should no longer be considered as belonging exclusively to basic science, but rather should be used for providing new insights in the clinical management of patients with endocrine autoimmune diseases.
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48

Świerczek, Artur, Krzysztof Pociecha, Hanna Plutecka, Marietta Ślusarczyk, Grażyna Chłoń-Rzepa, and Elżbieta Wyska. "Pharmacokinetic/Pharmacodynamic Evaluation of a New Purine-2,6-Dione Derivative in Rodents with Experimental Autoimmune Diseases." Pharmaceutics 14, no. 5 (May 19, 2022): 1090. http://dx.doi.org/10.3390/pharmaceutics14051090.

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Current treatment strategies of autoimmune diseases (ADs) display a limited efficacy and cause numerous adverse effects. Phosphodiesterase (PDE)4 and PDE7 inhibitors have been studied recently as a potential treatment of a variety of ADs. In this study, a PK/PD disease progression modeling approach was employed to evaluate effects of a new theophylline derivative, compound 34, being a strong PDE4 and PDE7 inhibitor. Activity of the studied compound against PDE1 and PDE3 in vitro was investigated. Animal models of multiple sclerosis (MS), rheumatoid arthritis (RA), and autoimmune hepatitis were utilized to assess the efficacy of this compound, and its pharmacokinetics was investigated in mice and rats. A new PK/PD disease progression model of compound 34 was developed that satisfactorily predicted the clinical score-time courses in mice with experimental encephalomyelitis that is an animal model of MS. Compound 34 displayed a high efficacy in all three animal models of ADs. Simultaneous inhibition of PDE types located in immune cells may constitute an alternative treatment strategy of ADs. The PK/PD encephalomyelitis and arthritis progression models presented in this study may be used in future preclinical research, and, upon modifications, may enable translation of the results of preclinical investigations into the clinical settings.
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49

Fan, Xueli, Chenhong Lin, Jinming Han, Xinmei Jiang, Jie Zhu, and Tao Jin. "Follicular Helper CD4+T Cells in Human Neuroautoimmune Diseases and Their Animal Models." Mediators of Inflammation 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/638968.

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Follicular helper CD4+T (TFH) cells play a fundamental role in humoral immunity deriving from their ability to provide help for germinal center (GC) formation, B cell differentiation into plasma cells and memory cells, and antibody production in secondary lymphoid tissues. TFH cells can be identified by a combination of markers, including the chemokine receptor CXCR5, costimulatory molecules ICOS and PD-1, transcription repressor Bcl-6, and cytokine IL-21. It is difficult and impossible to get access to secondary lymphoid tissues in humans, so studies are usually performed with human peripheral blood samples as circulating counterparts of tissue TFH cells. A balance of TFH cell generation and function is critical for protective antibody response, whereas overactivation of TFH cells or overexpression of TFH-associated molecules may result in autoimmune diseases. Emerging data have shown that TFH cells and TFH-associated molecules may be involved in the pathogenesis of neuroautoimmune diseases including multiple sclerosis (MS), neuromyelitis optica (NMO)/neuromyelitis optica spectrum disorders (NMOSD), and myasthenia gravis (MG). This review summarizes the features of TFH cells, including their development, function, and roles as well as TFH-associated molecules in neuroautoimmune diseases and their animal models.
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Iberg, Courtney A., and Daniel Hawiger. "Targeting Dendritic Cells with Antigen-Delivering Antibodies for Amelioration of Autoimmunity in Animal Models of Multiple Sclerosis and Other Autoimmune Diseases." Antibodies 9, no. 2 (June 15, 2020): 23. http://dx.doi.org/10.3390/antib9020023.

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The specific targeting of dendritic cells (DCs) using antigen-delivering antibodies has been established to be a highly efficient protocol for the induction of tolerance and protection from autoimmune processes in experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS), as well as in some other animal disease models. As the specific mechanisms of such induced tolerance are being investigated, the newly gained insights may also possibly help to design effective treatments for patients. Here we review approaches applied for the amelioration of autoimmunity in animal models based on antibody-mediated targeting of self-antigens to DCs. Further, we discuss relevant mechanisms of immunological tolerance that underlie such approaches, and we also offer some future perspectives for the application of similar methods in certain related disease settings such as transplantation.
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