Bibliographies thématiques / Experimental Autoimmune Encephalomyelitis, Progesterone / Articles de revues
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Articles de revues sur le sujet « Experimental Autoimmune Encephalomyelitis, Progesterone »

Auteur : Grafiati
Publié le 9 mars 2023
Mis à jour le 10 mars 2023

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1

Giatti, S., D. Caruso, M. Boraso, F. Abbiati, E. Ballarini, D. Calabrese, M. Pesaresi et al. « Neuroprotective Effects of Progesterone in Chronic Experimental Autoimmune Encephalomyelitis ». Journal of Neuroendocrinology 24, no 6 (10 mai 2012) : 851–61. http://dx.doi.org/10.1111/j.1365-2826.2012.02284.x.

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Garay, Laura, Maria Claudia Gonzalez Deniselle, Regine Sitruk-Ware, Rachida Guennoun, Michael Schumacher et Alejandro F. De Nicola. « Efficacy of the selective progesterone receptor agonist Nestorone for chronic experimental autoimmune encephalomyelitis ». Journal of Neuroimmunology 276, no 1-2 (novembre 2014) : 89–97. http://dx.doi.org/10.1016/j.jneuroim.2014.08.619.

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Yates, M. A., Y. Li, P. Chlebeck, T. Proctor, A. A. Vandenbark et H. Offner. « Progesterone treatment reduces disease severity and increases IL-10 in experimental autoimmune encephalomyelitis ». Journal of Neuroimmunology 220, no 1-2 (mars 2010) : 136–39. http://dx.doi.org/10.1016/j.jneuroim.2010.01.013.

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Garay, L. I., M. C. González Deniselle, M. E. Brocca, A. Lima, P. Roig et A. F. De Nicola. « Progesterone down-regulates spinal cord inflammatory mediators and increases myelination in experimental autoimmune encephalomyelitis ». Neuroscience 226 (décembre 2012) : 40–50. http://dx.doi.org/10.1016/j.neuroscience.2012.09.032.

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Garay, Laura, Maria Claudia Gonzalez Deniselle, Maria Meyer, Juan José Lopez Costa, Analia Lima, Paulina Roig et Alejandro F. DeNicola. « Protective effects of progesterone administration on axonal pathology in mice with experimental autoimmune encephalomyelitis ». Brain Research 1283 (août 2009) : 177–85. http://dx.doi.org/10.1016/j.brainres.2009.04.057.

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Utevska, S. V. « Experimental autoimmune encephalomyelitis (EAE) course in prenatally stressed rat males, the offspring of mothers with different sensitivity to EAE ». Faktori eksperimental'noi evolucii organizmiv 24 (30 août 2019) : 244–48. http://dx.doi.org/10.7124/feeo.v24.1109.

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Aim. The research is aimed at investigating the effect of prenatal stress on the incidence and course of experimental autoimmune encephalomyelitis (EAE) as well as the level of sex hormones in 200-days-old male rats, offspring of females with different sensitivity to EAE induction. Methods. The incidence and severity of EAE including duration of latent period, duration of the period from the first to the maximum manifestation of motor disfunction, mean clinical scores, maximum level of motor disfunction (maximum clinical scores) were analyzed in rats with induced EAE. Serum testosterone, estradiol and progesterone levels were measure during Enzyme-Linked Immunosorbent Assay (ELISA). Results. The estradiol level of prenatally stressed males was significantly lower than in rats from the control group. Sensitive to EAE test male rats had lower testosterone levels than EAE resistant males, and the offspring of EAE sensitive mothers were more resistant to EAE induction than the offspring of EAE resistant mothers. Conclusions. Without significant changes in the course of EAE, the reduction in incidence depends on a combination of factors such as mother's sensitivity to EAE induction and prenatal stress. Keywords: experimental autoimmune encephalomyelitis (EAE), prenatal stress, sex hormones, sensitivity to EAE induction.
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Yu, Hong-jun, Jun Fei, Xing-shu Chen, Qi-yan Cai, Hong-liang Liu, Guo-dong Liu et Zhong-xiang Yao. « Progesterone attenuates neurological behavioral deficits of experimental autoimmune encephalomyelitis through remyelination with nucleus-sublocalized Olig1 protein ». Neuroscience Letters 476, no 1 (mai 2010) : 42–45. http://dx.doi.org/10.1016/j.neulet.2010.03.079.

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Ghoumari, Abdel Mouman, Charly Abi Ghanem, Narimène Asbelaoui, Michael Schumacher et Rashad Hussain. « Roles of Progesterone, Testosterone and Their Nuclear Receptors in Central Nervous System Myelination and Remyelination ». International Journal of Molecular Sciences 21, no 9 (30 avril 2020) : 3163. http://dx.doi.org/10.3390/ijms21093163.

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Progesterone and testosterone, beyond their roles as sex hormones, are neuroactive steroids, playing crucial regulatory functions within the nervous system. Among these, neuroprotection and myelin regeneration are important ones. The present review aims to discuss the stimulatory effects of progesterone and testosterone on the process of myelination and remyelination. These effects have been demonstrated in vitro (i.e., organotypic cultures) and in vivo (cuprizone- or lysolecithin-induced demyelination and experimental autoimmune encephalomyelitis (EAE)). Both steroids stimulate myelin formation and regeneration by acting through their respective intracellular receptors: progesterone receptors (PR) and androgen receptors (AR). Activation of these receptors results in multiple events involving direct transcription and translation, regulating general homeostasis, cell proliferation, differentiation, growth and myelination. It also ameliorates immune response as seen in the EAE model, resulting in a significant decrease in inflammation leading to a fast recovery. Although natural progesterone and testosterone have a therapeutic potential, their synthetic derivatives—the 19-norprogesterone (nestorone) and 7α-methyl-nortestosterone (MENT), already used as hormonal contraception or in postmenopausal hormone replacement therapies, may offer enhanced benefits for myelin repair. We summarize here a recent advancement in the field of myelin biology, to treat demyelinating disorders using the natural as well as synthetic analogs of progesterone and testosterone.
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Engler, Jan Broder, Nina Kursawe, María Emilia Solano, Kostas Patas, Sabine Wehrmann, Nina Heckmann, Fred Lühder et al. « Glucocorticoid receptor in T cells mediates protection from autoimmunity in pregnancy ». Proceedings of the National Academy of Sciences 114, no 2 (3 janvier 2017) : E181—E190. http://dx.doi.org/10.1073/pnas.1617115114.

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Pregnancy is one of the strongest inducers of immunological tolerance. Disease activity of many autoimmune diseases including multiple sclerosis (MS) is temporarily suppressed by pregnancy, but little is known about the underlying molecular mechanisms. Here, we investigated the endocrine regulation of conventional and regulatory T cells (Tregs) during reproduction. In vitro, we found the pregnancy hormone progesterone to robustly increase Treg frequencies via promiscuous binding to the glucocorticoid receptor (GR) in T cells. In vivo, T-cell–specific GR deletion in pregnant animals undergoing experimental autoimmune encephalomyelitis (EAE), the animal model of MS, resulted in a reduced Treg increase and a selective loss of pregnancy-induced protection, whereas reproductive success was unaffected. Our data imply that steroid hormones can shift the immunological balance in favor of Tregs via differential engagement of the GR in T cells. This newly defined mechanism confers protection from autoimmunity during pregnancy and represents a potential target for future therapy.
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Goudarzvand, Mahdi, Yaser Panahi, Reza Yazdani, Hosein Miladi, Saeed Tahmasebi, Amin Sherafat, Sanaz Afraei et al. « The Effects of D-aspartate on Neurosteroids, Neurosteroid Receptors, and Inflammatory Mediators in Experimental Autoimmune Encephalomyelitis ». Endocrine, Metabolic & ; Immune Disorders - Drug Targets 19, no 3 (15 avril 2019) : 316–25. http://dx.doi.org/10.2174/1871530318666181005093459.

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Objective: Experimental autoimmune encephalomyelitis (EAE) is a widely used model for multiple sclerosis. The present study has been designed to compare the efficiencies of oral and intraperitoneal (IP) administration of D-aspartate (D-Asp) on the onset and severity of EAE, the production of neurosteroids, and the expression of neurosteroid receptors and inflammatory mediators in the brain of EAE mice. Methods: In this study, EAE was induced in C57BL/6 mice treated with D-Asp orally (D-Asp-Oral) or by IP injection (D-Asp-IP). On the 20th day, brains (cerebrums) and cerebellums of mice were evaluated by histological analyses. The brains of mice were analyzed for: 1) Neurosteroid (Progesterone, Testosterone, 17β-estradiol) concentrations; 2) gene expressions of cytokines and neurosteroid receptors by reverse transcription polymerase chain reaction, and 3) quantitative determination of D-Asp using liquid chromatography-tandem mass spectrometry. Further, some inflammatory cytokines and matrix metalloproteinase-2 (MMP-2) were identified in the mouse serum using enzyme-linked immunosorbent assay kits. Results: Our findings demonstrated that after D-Asp was administered, it was taken up and accumulated within the brain. Further, IP injection of D-Asp had more beneficial effects on EAE severity than oral gavage. The concentration of the testosterone and 17β-estradiol in D-Asp-IP group was significantly higher than that of the control group. There were no significant differences in the gene expression of cytokine and neurosteroid receptors between control, D-Asp-IP, and D-Asp-Oral groups. However, IP treatment with D-Asp significantly reduced C-C motif chemokine ligand 2 and MMP-2 serum levels compared to control mice. Conclusion: IP injection of D-Asp had more beneficial effects on EAE severity, neurosteroid induction and reduction of inflammatory mediators than oral gavage.
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Kanellopoulos, Jean. « Experimental autoimmune encephalomyelitis ». Biomedical Journal 38, no 3 (2015) : 181. http://dx.doi.org/10.4103/2319-4170.158500.

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&NA;. « ?? ? and experimental autoimmune encephalomyelitis ». Inpharma Weekly &NA;, no 1051 (août 1996) : 8. http://dx.doi.org/10.2165/00128413-199610510-00018.

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Glynn, P., D. Weedon et M. L. Cuzner. « Chronic experimental autoimmune encephalomyelitis ». Journal of the Neurological Sciences 73, no 1 (mars 1986) : 111–23. http://dx.doi.org/10.1016/0022-510x(86)90069-9.

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HEININGER, KURT, WALTER FIERZ, BÄRBEL SCHÄFER, HANS-PETER HARTUNG et KLAUS V. TOYKA. « Adoptive Transfer Experimental Autoimmune Encephalomyelitis. » Annals of the New York Academy of Sciences 540, no 1 Advances in N (novembre 1988) : 738–40. http://dx.doi.org/10.1111/j.1749-6632.1988.tb27231.x.

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Dal Canto, R., G. Costa, L. Steinman, M. Dal Canto et C. G. Fathman. « Experimental “autoimmune” versus “allergic” encephalomyelitis ». Journal of Neuroimmunology 90, no 1 (septembre 1998) : 4. http://dx.doi.org/10.1016/s0165-5728(98)91215-2.

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Weedon, D., P. Glynn et M. L. Cuzner. « Chronic relapsing experimental autoimmune encephalomyelitis ». Journal of the Neurological Sciences 72, no 2-3 (février 1986) : 255–63. http://dx.doi.org/10.1016/0022-510x(86)90013-4.

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W., Li, L. Quigley, D. L. Yao, L. D. Hudson, M. Brenner, B. J. Zhang, S. Brocke, H. F. McFarland et H. DeF Webster. « Chronic Relapsing Experimental Autoimmune Encephalomyelitis ». Journal of Neuropathology and Experimental Neurology 57, no 5 (mai 1998) : 426–38. http://dx.doi.org/10.1097/00005072-199805000-00006.

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Varriale, S., E. Béraud, D. Brandli, J. Barbaria, M. M. Golstein et D. Bernard. « Regulation of experimental autoimmune encephalomyelitis ». Journal of Neuroimmunology 22, no 1 (mars 1989) : 31–40. http://dx.doi.org/10.1016/0165-5728(89)90006-4.

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Sternberg, Z., A. Cesario, K. Rittenhouse-Olson, R. A. Sobel, O. Pankewycz, B. Zhu, T. Whitcomb, D. S. Sternberg et F. E. Munschauer. « Acamprosate modulates experimental autoimmune encephalomyelitis ». Inflammopharmacology 20, no 1 (17 novembre 2011) : 39–48. http://dx.doi.org/10.1007/s10787-011-0097-1.

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Anderton, StephenM. « Peptide immunotherapy in experimental autoimmune encephalomyelitis ». Biomedical Journal 38, no 3 (2015) : 206. http://dx.doi.org/10.4103/2319-4170.158510.

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Nam, Ki Hoan. « Experimental autoimmune encephalomyelitis in cynomolgus monkeys ». Journal of Veterinary Science 1, no 2 (2000) : 127. http://dx.doi.org/10.4142/jvs.2000.1.2.127.

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Feinstein, D. L., C. F. Brosnan, C. C. Whitacre, G. E. Landreth, V. Gavrilyuk et M. T. Heneka. « PPAR-agonists prevent experimental autoimmune encephalomyelitis ». Journal of Neurochemistry 81 (28 juin 2008) : 36. http://dx.doi.org/10.1046/j.1471-4159.81.s1.81.x.

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Rodrigues, David Henrique, Daniela Sachs et Antonio Lucio Teixeira. « Mechanical hypernociception in experimental autoimmune encephalomyelitis ». Arquivos de Neuro-Psiquiatria 67, no 1 (mars 2009) : 78–81. http://dx.doi.org/10.1590/s0004-282x2009000100019.

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BACKGROUND: Pain is an important clinical manifestation in multiple sclerosis (MS) patients, though it has been neglected in clinical and experimental researches. OBJECTIVE: To investigate the nociceptive response in MOG35-55 experimental autoimmune encephalomyelitis (EAE)-induced mice. METHOD: EAE was induced in 8 to 10 week old C57BL/6 female mice with an emulsion of MOG35-55, Complete Freund Adjuvant, Mycobacterium tuberculosis H37 RA and pertussis toxin. Nociception was evaluated by the von Frey filaments method. A clinical scale ranging from 0 to 15 was used to assess motor impairment. RESULTS: Clinical evidence of disease started at day 10 and peaked at day 14 after immunization. Thereafter, there was no worsening of symptoms until day 26. The EAE-induced mice presented reduced pressure threshold at days 7th and 10th after immunization and before the onset of clinical motor signs. CONCLUSION : The hypernociception found validates MOG35-55 EAE as a model for the study of pain in multiple sclerosis.
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Novikova, Natalia S., Anastasia S. Diatlova, Kristina Z. Derevtsova, Elena A. Korneva, Tamara V. Viktorovna, Yuri Ostrinki, Lital Abraham et al. « Tuftsin-phosphorylcholine attenuate experimental autoimmune encephalomyelitis ». Journal of Neuroimmunology 337 (décembre 2019) : 577070. http://dx.doi.org/10.1016/j.jneuroim.2019.577070.

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WHITACRE, CAROLINE C., KENNICHI DOWDELL et ANN C. GRIFFIN. « Neuroendocrine Influences on Experimental Autoimmune Encephalomyelitis ». Annals of the New York Academy of Sciences 840, no 1 (mai 1998) : 705–16. http://dx.doi.org/10.1111/j.1749-6632.1998.tb09609.x.

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Pollak, Yehuda, Haim Ovadia, Inbal Goshen, Ronnie Gurevich, Keren Monsa, Ronit Avitsur et Raz Yirmiya. « Behavioral aspects of experimental autoimmune encephalomyelitis ». Journal of Neuroimmunology 104, no 1 (avril 2000) : 31–36. http://dx.doi.org/10.1016/s0165-5728(99)00257-x.

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Pelfrey, Clara M., Frank J. Waxman et Caroline C. Whitacre. « Genetic resistance in experimental autoimmune encephalomyelitis ». Cellular Immunology 122, no 2 (septembre 1989) : 504–16. http://dx.doi.org/10.1016/0008-8749(89)90096-8.

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Baker, David, et Sandra Amor. « Quality control of experimental autoimmune encephalomyelitis ». Multiple Sclerosis Journal 16, no 9 (septembre 2010) : 1025–27. http://dx.doi.org/10.1177/1352458510378317.

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Inada, Rino, Katsuichi Miyamoto, Noriko Tanaka, Kota Moriguchi et Susumu Kusunoki. « Oryeongsan (Goreisan) Ameliorates Experimental Autoimmune Encephalomyelitis ». Internal Medicine 59, no 1 (1 janvier 2020) : 55–60. http://dx.doi.org/10.2169/internalmedicine.3030-19.

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WHITACRE, CAROLINE C., INGRID E. GIENAPP, ABBIE MEYER, KAREN L. COX et NAJMA JAVED. « Oral Tolerance in Experimental Autoimmune Encephalomyelitis ». Annals of the New York Academy of Sciences 778, no 1 (février 1996) : 217–27. http://dx.doi.org/10.1111/j.1749-6632.1996.tb21130.x.

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JAVED, NAJMA H., INGRID GIENAPP, KAREN COX et CAROLINE C. WHITACRE. « Oral Tolerance in Experimental Autoimmune Encephalomyelitis. » Annals of the New York Academy of Sciences 778, no 1 (février 1996) : 393–94. http://dx.doi.org/10.1111/j.1749-6632.1996.tb21154.x.

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Bernstein, Alison I., et Gary W. Miller. « Oxidative Signaling in Experimental Autoimmune Encephalomyelitis ». Toxicological Sciences 114, no 2 (avril 2010) : 159–61. http://dx.doi.org/10.1093/toxsci/kfq012.

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Ueno, Rino, Katsuichi Miyamoto, Noriko Tanaka, Kota Moriguchi, Kenji Kadomatsu et Susumu Kusunoki. « Keratan sulfate exacerbates experimental autoimmune encephalomyelitis ». Journal of Neuroscience Research 93, no 12 (5 septembre 2015) : 1874–80. http://dx.doi.org/10.1002/jnr.23640.

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Swanborg, R. H., K. E. Gould et J. A. Stepaniak. « Studies of experimental autoimmune encephalomyelitis (EAE) ». Journal of Immunology 153, no 5 (1 septembre 1994) : 2352. http://dx.doi.org/10.4049/jimmunol.153.5.2352.

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Hoffman, Kristina R., David P. Daberkow, Hannah M. Kohl, Tyrel Long, Trevor O. Kirby et Javier Ochoa-Reparaz. « Microbiome methods in experimental autoimmune encephalomyelitis. » Journal of Immunology 208, no 1_Supplement (1 mai 2022) : 158.13. http://dx.doi.org/10.4049/jimmunol.208.supp.158.13.

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Abstract Multiple Sclerosis (MS) is an autoimmune disease that affects the central nervous system (CNS) via neuroinflammation and demyelination. The exact triggers, subsets and effector mechanisms that contribute to disease progression are still largely unknown. Recent studies of healthy vs MS human stool samples indicated an altered microbiome, dysbiosis, which could lead to inflammation and disease. Experimental autoimmune encephalomyelitis (EAE) is a model used for the study of MS and can be induced in multiple non-rodent and rodent species. It is critical to control the environment of both the animal facility and experimental housing conditions in microbiome studies. We compared commercial vendors, Envigo and Jackson Laboratory, C57BL/6 female mice. Fecal samples were collected at Day 0, 14, and 21 for DNA extraction and sequencing of the ribosomal DNA (rDNA) to analyze the gut microbiome composition prior to and after induction of EAE. There was a significant difference between sources with Jackson Laboratory mice having an increased severity index compared to Envigo mice (p < 0.01) and a decreased survival rate of 20% when compared to 85% for Envigo mice. Our results suggest different sources of EAE mouse models have critical impacts on microbiome composition and levels of disease severity. Furthermore, this highlights the importance of consistent and controlled conditions from the animal model source, and throughout the experiment, when inducing EAE in mice and other animal models of disease. This project was sponsored by NIH grant R15 NS107743.
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Hou, Lifei, Florian Winau et Eileen Remold-O’Donnell. « SerpinB1 Deficiency Ameliorates Experimental Autoimmune Encephalomyelitis ». Journal of Immunology 196, no 1_Supplement (1 mai 2016) : 58.13. http://dx.doi.org/10.4049/jimmunol.196.supp.58.13.

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Abstract Increasing evidence shows that, in autoimmune settings, Th17 cells are converted to pathogenic Th17 cells (patho-Th17), which produce GM-CSF and IFNγ and are pivotal for pathogenesis. We recently discovered that serpinB1, a protease inhibitor, is the signature gene of Th17 cells and forms a regulatory module with cathepsin L that controls Th17 cell generation: Th17 differentiation is restricted by serpinB1 and counter-regulated by cathepsin L. In the current study, we investigated serpinB1 regulation of Th17 cell pathogenicity in experimental autoimmune encephalomyelitis (EAE). As anticipated, expression of serpinB1 and other Th17 genes were significantly increased in effector CD4 cells in the EAE mouse. Surprisingly, serpinB1 deficient (sb1−/−) mice immunized with MOG35–55 are resistant to EAE, manifested by dramatically decreased disease incidence and severity. Adoptive transfer experiments showed that the protective effect of serpinB1 deficiency is CD4 cell specific. Cytokine profiling showed that, despite producing more Th17 cells, serpinB1 deficiency selectively diminished patho-Th17 cells. Furthermore, Ki-67 and Annexin V staining together with BrdU pulse/chase strategy confirmed that proliferation is not defective in sb1−/− Th17 and patho-Th17 cells. In contrast, sb1−/− patho-Th17 cells showed significantly shortened life span and were eliminated upon antigen-recall. Finally, in vivo administration of E64D, a broad-acting cysteine protease inhibitor, partially reversed the effects of serpinB1 deficiency. Thus, our study identified a protease-protease inhibitor regulatory module acting on Th17 cell differentiation and separately on pathogenicity with potential for targeting in autoimmune diseases.
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Varriale, S., E. Béraud, J. Barbaria, R. Galibert et D. Bernard. « Regulation of experimental autoimmune encephalomyelitis : Inhibition of adoptive experimental autoimmune encephalomyelitis by ‘recovery-associated suppressor cells’ ». Journal of Neuroimmunology 53, no 2 (septembre 1994) : 123–31. http://dx.doi.org/10.1016/0165-5728(94)90022-1.

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Shin, Taekyun, Meejung Ahn, Changjong Moon et Seungjoon Kim. « Erythropoietin and autoimmune neuroinflammation : lessons from experimental autoimmune encephalomyelitis and experimental autoimmune neuritis ». Anatomy & ; Cell Biology 45, no 4 (2012) : 215. http://dx.doi.org/10.5115/acb.2012.45.4.215.

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Ahn, Meejung, Jeongtae Kim, Wonjun Yang, Yuna Choi, Poornima Ekanayake, Hyunju Ko, Youngheun Jee et Taekyun Shin. « Amelioration of experimental autoimmune encephalomyelitis byIshige okamurae ». Anatomy & ; Cell Biology 51, no 4 (2018) : 292. http://dx.doi.org/10.5115/acb.2018.51.4.292.

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De Sarno, Patrizia, Robert C. Axtell, Chander Raman, Kevin A. Roth, Dario R. Alessi et Richard S. Jope. « Lithium Prevents and Ameliorates Experimental Autoimmune Encephalomyelitis ». Journal of Immunology 181, no 1 (19 juin 2008) : 338–45. http://dx.doi.org/10.4049/jimmunol.181.1.338.

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Theil, Michael-Mark, Sachiko Miyake, Miho Mizuno, Chiharu Tomi, J. Ludovic Croxford, Hiroshi Hosoda, Julia Theil et al. « Suppression of Experimental Autoimmune Encephalomyelitis by Ghrelin ». Journal of Immunology 183, no 4 (20 juillet 2009) : 2859–66. http://dx.doi.org/10.4049/jimmunol.0803362.

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Mausner-Fainberg, Karin. « Eotaxin-2 blockade ameliorates experimental autoimmune encephalomyelitis ». World Journal of Immunology 3, no 1 (2013) : 7. http://dx.doi.org/10.5411/wji.v3.i1.7.

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Murugaiyan, Gopal, Vanessa Beynon, Akanksha Mittal, Nicole Joller et Howard L. Weiner. « Silencing MicroRNA-155 Ameliorates Experimental Autoimmune Encephalomyelitis ». Journal of Immunology 187, no 5 (25 juillet 2011) : 2213–21. http://dx.doi.org/10.4049/jimmunol.1003952.

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Le, Thuong Manh, Mika Takarada-Iemata, Hieu Minh Ta, Jureepon Roboon, Hiroshi Ishii, Takashi Tamatani, Yasuko Kitao, Tsuyoshi Hattori et Osamu Hori. « Ndrg2deficiency ameliorates neurodegeneration in experimental autoimmune encephalomyelitis ». Journal of Neurochemistry 145, no 2 (19 février 2018) : 139–53. http://dx.doi.org/10.1111/jnc.14294.

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Piccio, Laura, Jennifer L. Stark et Anne H. Cross. « Chronic calorie restriction attenuates experimental autoimmune encephalomyelitis ». Journal of Leukocyte Biology 84, no 4 (4 août 2008) : 940–48. http://dx.doi.org/10.1189/jlb.0208133.

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Namiki, Kana, Hirofumi Matsunaga, Kento Yoshioka, Kensuke Tanaka, Kazuya Murata, Junji Ishida, Akira Sakairi et al. « Mechanism for p38α-mediated Experimental Autoimmune Encephalomyelitis ». Journal of Biological Chemistry 287, no 29 (25 mai 2012) : 24228–38. http://dx.doi.org/10.1074/jbc.m111.338541.

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Prosiegel, M., I. Neu, S. Vogl, G. Hoffmann, A. Wildfeuer et G. Ruhenstroth-Bauer. « Suppression of experimental autoimmune encephalomyelitis by sulfasalazine ». Acta Neurologica Scandinavica 81, no 3 (29 janvier 2009) : 237–38. http://dx.doi.org/10.1111/j.1600-0404.1990.tb00973.x.

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BATOULIS, HELENA, MASCHA S. RECKS, KLAUS ADDICKS et STEFANIE KUERTEN. « Experimental autoimmune encephalomyelitis - achievements and prospective advances ». APMIS 119, no 12 (18 octobre 2011) : 819–30. http://dx.doi.org/10.1111/j.1600-0463.2011.02794.x.

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Witting, A., L. Chen, E. Cudaback, A. Straiker, L. Walter, B. Rickman, T. Moller, C. Brosnan et N. Stella. « Experimental autoimmune encephalomyelitis disrupts endocannabinoid-mediated neuroprotection ». Proceedings of the National Academy of Sciences 103, no 16 (29 mars 2006) : 6362–67. http://dx.doi.org/10.1073/pnas.0510418103.

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ABREU, SERGIO L., IMMAC THAMPOE et PAUL KAPLAN. « Interferon in Experimental Autoimmune Encephalomyelitis : Intraventricular Administration ». Journal of Interferon Research 6, no 6 (décembre 1986) : 627–32. http://dx.doi.org/10.1089/jir.1986.6.627.

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