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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 31 juillet 2025

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1

Giatti, S., D. Caruso, M. Boraso, et al. "Neuroprotective Effects of Progesterone in Chronic Experimental Autoimmune Encephalomyelitis." Journal of Neuroendocrinology 24, no. 6 (2012): 851–61. http://dx.doi.org/10.1111/j.1365-2826.2012.02284.x.

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Milosevic, Ana, Irena Lavrnja, Danijela Savic, et al. "Rat Ovarian Function Is Impaired during Experimental Autoimmune Encephalomyelitis." Cells 12, no. 7 (2023): 1045. http://dx.doi.org/10.3390/cells12071045.

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Multiple sclerosis (MS) is an autoimmune disease affecting the CNS and occurring far more prevalently in women than in men. In both MS and its animal models, sex hormones play important immunomodulatory roles. We have previously shown that experimental autoimmune encephalomyelitis (EAE) affects the hypothalamic–pituitary–gonadal axis in rats of both sexes and induces an arrest in the estrous cycle in females. To investigate the gonadal status in female rats with EAE, we explored ovarian morphometric parameters, circulating and intraovarian sex steroid levels, and the expression of steroidogeni

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3

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

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4

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

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5

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

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6

Garay, Laura, Maria Claudia Gonzalez Deniselle, Maria Meyer, et al. "Protective effects of progesterone administration on axonal pathology in mice with experimental autoimmune encephalomyelitis." Brain Research 1283 (August 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 (August 30, 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, estra

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Milosevic, Ana, Katarina Milosevic, Anica Zivkovic, et al. "Alterations in the Hypothalamic–Pituitary–Adrenal Axis as a Response to Experimental Autoimmune Encephalomyelitis in Dark Agouti Rats of Both Sexes." Biomolecules 14, no. 8 (2024): 1020. http://dx.doi.org/10.3390/biom14081020.

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Multiple sclerosis (MS) is a chronic inflammatory disease that affects the central nervous system, usually diagnosed during the reproductive period. Both MS and its commonly used animal model, experimental autoimmune encephalomyelitis (EAE), exhibit sex-specific features regarding disease progression and disturbances in the neuroendocrine and endocrine systems. This study investigates the hypothalamic–pituitary–adrenal (HPA) axis response of male and female Dark Agouti rats during EAE. At the onset of EAE, Crh expression in the hypothalamus of both sexes is decreased, while males show reduced

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9

Yu, Hong-jun, Jun Fei, Xing-shu Chen, et al. "Progesterone attenuates neurological behavioral deficits of experimental autoimmune encephalomyelitis through remyelination with nucleus-sublocalized Olig1 protein." Neuroscience Letters 476, no. 1 (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, and 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 (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 formati

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11

Engler, Jan Broder, Nina Kursawe, María Emilia Solano, et al. "Glucocorticoid receptor in T cells mediates protection from autoimmunity in pregnancy." Proceedings of the National Academy of Sciences 114, no. 2 (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

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12

Goudarzvand, Mahdi, Yaser Panahi, Reza Yazdani, 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 (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 eva

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13

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 (1996): 8. http://dx.doi.org/10.2165/00128413-199610510-00018.

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15

Glynn, P., D. Weedon, and M. L. Cuzner. "Chronic experimental autoimmune encephalomyelitis." Journal of the Neurological Sciences 73, no. 1 (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, and KLAUS V. TOYKA. "Adoptive Transfer Experimental Autoimmune Encephalomyelitis." Annals of the New York Academy of Sciences 540, no. 1 Advances in N (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, and C. G. Fathman. "Experimental “autoimmune” versus “allergic” encephalomyelitis." Journal of Neuroimmunology 90, no. 1 (1998): 4. http://dx.doi.org/10.1016/s0165-5728(98)91215-2.

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18

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

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19

W., Li, L. Quigley, D. L. Yao, et al. "Chronic Relapsing Experimental Autoimmune Encephalomyelitis." Journal of Neuropathology and Experimental Neurology 57, no. 5 (1998): 426–38. http://dx.doi.org/10.1097/00005072-199805000-00006.

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20

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

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21

Sternberg, Z., A. Cesario, K. Rittenhouse-Olson, et al. "Acamprosate modulates experimental autoimmune encephalomyelitis." Inflammopharmacology 20, no. 1 (2011): 39–48. http://dx.doi.org/10.1007/s10787-011-0097-1.

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22

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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23

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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24

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

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25

Rodrigues, David Henrique, Daniela Sachs, and Antonio Lucio Teixeira. "Mechanical hypernociception in experimental autoimmune encephalomyelitis." Arquivos de Neuro-Psiquiatria 67, no. 1 (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. RE

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26

Novikova, Natalia S., Anastasia S. Diatlova, Kristina Z. Derevtsova, et al. "Tuftsin-phosphorylcholine attenuate experimental autoimmune encephalomyelitis." Journal of Neuroimmunology 337 (December 2019): 577070. http://dx.doi.org/10.1016/j.jneuroim.2019.577070.

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27

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

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28

Pollak, Yehuda, Haim Ovadia, Inbal Goshen, et al. "Behavioral aspects of experimental autoimmune encephalomyelitis." Journal of Neuroimmunology 104, no. 1 (2000): 31–36. http://dx.doi.org/10.1016/s0165-5728(99)00257-x.

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29

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

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30

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

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31

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

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32

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

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Bernstein, Alison I., and Gary W. Miller. "Oxidative Signaling in Experimental Autoimmune Encephalomyelitis." Toxicological Sciences 114, no. 2 (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, and Susumu Kusunoki. "Keratan sulfate exacerbates experimental autoimmune encephalomyelitis." Journal of Neuroscience Research 93, no. 12 (2015): 1874–80. http://dx.doi.org/10.1002/jnr.23640.

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Swanborg, R. H., K. E. Gould, and J. A. Stepaniak. "Studies of experimental autoimmune encephalomyelitis (EAE)." Journal of Immunology 153, no. 5 (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, and Javier Ochoa-Reparaz. "Microbiome methods in experimental autoimmune encephalomyelitis." Journal of Immunology 208, no. 1_Supplement (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

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38

Hou, Lifei, Florian Winau, and Eileen Remold-O’Donnell. "SerpinB1 Deficiency Ameliorates Experimental Autoimmune Encephalomyelitis." Journal of Immunology 196, no. 1_Supplement (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 ant

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Varriale, S., E. Béraud, J. Barbaria, R. Galibert, and D. Bernard. "Regulation of experimental autoimmune encephalomyelitis: Inhibition of adoptive experimental autoimmune encephalomyelitis by ‘recovery-associated suppressor cells’." Journal of Neuroimmunology 53, no. 2 (1994): 123–31. http://dx.doi.org/10.1016/0165-5728(94)90022-1.

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40

Shin, Taekyun, Meejung Ahn, Changjong Moon, and 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, et al. "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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42

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

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43

Theil, Michael-Mark, Sachiko Miyake, Miho Mizuno, et al. "Suppression of Experimental Autoimmune Encephalomyelitis by Ghrelin." Journal of Immunology 183, no. 4 (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, and Howard L. Weiner. "Silencing MicroRNA-155 Ameliorates Experimental Autoimmune Encephalomyelitis." Journal of Immunology 187, no. 5 (2011): 2213–21. http://dx.doi.org/10.4049/jimmunol.1003952.

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Le, Thuong Manh, Mika Takarada-Iemata, Hieu Minh Ta, et al. "Ndrg2deficiency ameliorates neurodegeneration in experimental autoimmune encephalomyelitis." Journal of Neurochemistry 145, no. 2 (2018): 139–53. http://dx.doi.org/10.1111/jnc.14294.

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

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Namiki, Kana, Hirofumi Matsunaga, Kento Yoshioka та ін. "Mechanism for p38α-mediated Experimental Autoimmune Encephalomyelitis". Journal of Biological Chemistry 287, № 29 (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, and G. Ruhenstroth-Bauer. "Suppression of experimental autoimmune encephalomyelitis by sulfasalazine." Acta Neurologica Scandinavica 81, no. 3 (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, and STEFANIE KUERTEN. "Experimental autoimmune encephalomyelitis - achievements and prospective advances." APMIS 119, no. 12 (2011): 819–30. http://dx.doi.org/10.1111/j.1600-0463.2011.02794.x.

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