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Journal articles on the topic 'Experimental Autoimmune Encephalomyelitis, Progesterone'

Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 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 (May 10, 2012): 851–61. http://dx.doi.org/10.1111/j.1365-2826.2012.02284.x.

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2

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 (November 2014): 89–97. http://dx.doi.org/10.1016/j.jneuroim.2014.08.619.

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3

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 (March 2010): 136–39. http://dx.doi.org/10.1016/j.jneuroim.2010.01.013.

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4

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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5

Garay, Laura, Maria Claudia Gonzalez Deniselle, Maria Meyer, Juan José Lopez Costa, Analia Lima, Paulina Roig, and Alejandro F. DeNicola. "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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6

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, 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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7

Yu, Hong-jun, Jun Fei, Xing-shu Chen, Qi-yan Cai, Hong-liang Liu, Guo-dong Liu, and Zhong-xiang Yao. "Progesterone attenuates neurological behavioral deficits of experimental autoimmune encephalomyelitis through remyelination with nucleus-sublocalized Olig1 protein." Neuroscience Letters 476, no. 1 (May 2010): 42–45. http://dx.doi.org/10.1016/j.neulet.2010.03.079.

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8

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 (April 30, 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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9

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 (January 3, 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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10

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 (April 15, 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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11

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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12

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

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13

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

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14

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 (November 1988): 738–40. http://dx.doi.org/10.1111/j.1749-6632.1988.tb27231.x.

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15

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 (September 1998): 4. http://dx.doi.org/10.1016/s0165-5728(98)91215-2.

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16

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

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17

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

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18

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 (March 1989): 31–40. http://dx.doi.org/10.1016/0165-5728(89)90006-4.

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19

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

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20

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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21

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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22

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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23

Rodrigues, David Henrique, Daniela Sachs, and Antonio Lucio Teixeira. "Mechanical hypernociception in experimental autoimmune encephalomyelitis." Arquivos de Neuro-Psiquiatria 67, no. 1 (March 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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24

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 (December 2019): 577070. http://dx.doi.org/10.1016/j.jneuroim.2019.577070.

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25

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 (May 1998): 705–16. http://dx.doi.org/10.1111/j.1749-6632.1998.tb09609.x.

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26

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

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27

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

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28

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

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29

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

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30

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 (February 1996): 217–27. http://dx.doi.org/10.1111/j.1749-6632.1996.tb21130.x.

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31

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 (February 1996): 393–94. http://dx.doi.org/10.1111/j.1749-6632.1996.tb21154.x.

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32

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

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33

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 (September 5, 2015): 1874–80. http://dx.doi.org/10.1002/jnr.23640.

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34

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

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35

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 (May 1, 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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36

Hou, Lifei, Florian Winau, and Eileen Remold-O’Donnell. "SerpinB1 Deficiency Ameliorates Experimental Autoimmune Encephalomyelitis." Journal of Immunology 196, no. 1_Supplement (May 1, 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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37

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 (September 1994): 123–31. http://dx.doi.org/10.1016/0165-5728(94)90022-1.

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38

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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39

Ahn, Meejung, Jeongtae Kim, Wonjun Yang, Yuna Choi, Poornima Ekanayake, Hyunju Ko, Youngheun Jee, and 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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40

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 (June 19, 2008): 338–45. http://dx.doi.org/10.4049/jimmunol.181.1.338.

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41

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 (July 20, 2009): 2859–66. http://dx.doi.org/10.4049/jimmunol.0803362.

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42

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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43

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 (July 25, 2011): 2213–21. http://dx.doi.org/10.4049/jimmunol.1003952.

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44

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

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45

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

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46

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 (May 25, 2012): 24228–38. http://dx.doi.org/10.1074/jbc.m111.338541.

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47

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 (January 29, 2009): 237–38. http://dx.doi.org/10.1111/j.1600-0404.1990.tb00973.x.

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48

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

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49

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

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50

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

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