Persistent inflammation in the CNS during chronic EAE despite local absence of IL-17 production

التفاصيل البيبلوغرافية
العنوان: Persistent inflammation in the CNS during chronic EAE despite local absence of IL-17 production
المؤلفون: Larissa Camargo da Rosa, Larissa Lumi Watanabe Ishikawa, Camila Marques, Alexandrina Sartori, Sofia Fernanda Gonçalves Zorzella-Pezavento, Maura Rosane Valerio Ikoma, Thais Graziela Donegá França, Fernanda Chiuso-Minicucci
المساهمون: Universidade Estadual Paulista (Unesp), Laboratório de Citometria de Fluxo-Fundação
المصدر: Mediators of Inflammation
Scopus
Repositório Institucional da UNESP
Universidade Estadual Paulista (UNESP)
instacron:UNESP
Mediators of Inflammation, Vol 2013 (2013)
سنة النشر: 2013
مصطلحات موضوعية: Central Nervous System, cell infiltration, Encephalomyelitis, Freund's Adjuvant, animal cell, myelin oligodendrocyte glycoprotein, Mice, allergic encephalomyelitis, regulatory T lymphocyte, immune system diseases, nervous system inflammation, biology, Freund adjuvant, Experimental autoimmune encephalomyelitis, Interleukin-17, FOXP3, Forkhead Transcription Factors, female, medicine.anatomical_structure, priority journal, cytokine production, disease severity, Female, gamma interferon, Interleukin 17, lcsh:RB1-214, Research Article, Encephalomyelitis, Autoimmune, Experimental, Multiple Sclerosis, Article Subject, inflammatory infiltrate, animal experiment, Immunology, transcription factor FOXP3, Spleen, Myelin oligodendrocyte glycoprotein, body weight, Interferon-gamma, lcsh:Pathology, medicine, Animals, controlled study, mouse, Inflammation, nonhuman, pertussis toxin, animal model, Multiple sclerosis, Interleukin-2 Receptor alpha Subunit, scoring system, Cell Biology, Th1 Cells, medicine.disease, Mice, Inbred C57BL, Gene Expression Regulation, Freund's adjuvant, biology.protein, Th17 Cells, weight reduction, interleukin 17, spleen cell
الوصف: Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-27T11:29:58Z No. of bitstreams: 0Bitstream added on 2014-05-27T14:32:44Z : No. of bitstreams: 1 2-s2.0-84880150391.pdf: 4965419 bytes, checksum: 5f8946d795d9899f9e98251390cc4302 (MD5) Made available in DSpace on 2014-05-27T11:29:58Z (GMT). No. of bitstreams: 0 Previous issue date: 2013-07-19 Experimental autoimmune encephalomyelitis (EAE) is an artificially induced demyelination of the central nervous system (CNS) that resembles multiple sclerosis in its clinical, histopathological, and immunological features. Activated Th1 and Th17 cells are thought to be the main immunological players during EAE development. This study was designed to evaluate peripheral and local contribution of IL-17 to acute and chronic EAE stages. C57BL/6 mice were immunized with MOG plus complete Freund's adjuvant followed by pertussis toxin. Mice presented an initial acute phase characterized by accentuated weight loss and high clinical score, followed by a partial recovery when the animals reached normal body weight and smaller clinical scores. Spleen cells stimulated with MOG produced significantly higher levels of IFN-γ during the acute period whereas similar IL-17 levels were produced during both disease stages. CNS-infiltrating cells stimulated with MOG produced similar amounts of IFN-γ but, IL-17 was produced only at the acute phase of EAE. The percentage of Foxp3+ Treg cells, at the spleen and CNS, was elevated during both phases. The degree of inflammation was similar at both disease stages. Partial clinical recovery observed during chronic EAE was associated with no IL-17 production and presence of Foxp3+ Treg cells in the CNS. © 2013 Sofia Fernanda Gonçalves Zorzella-Pezavento et al. Department of Microbiology and Immunology Biosciences Institute Universidade Estadual Paulista (UNESP), 18618-070 Botucatu, SP Laboratório de Citometria de Fluxo-Fundação, Dr. Amaral Carvalho, Jaú, SP Department of Microbiology and Immunology Biosciences Institute Universidade Estadual Paulista (UNESP), 18618-070 Botucatu, SP
وصف الملف: text/xhtml
تدمد: 1466-1861
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::36100e8032a20710786ed51d4f413a69Test
https://pubmed.ncbi.nlm.nih.gov/23970813Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....36100e8032a20710786ed51d4f413a69
قاعدة البيانات: OpenAIRE