Lack of requirement for CD8+ cells in recovery from and resistance to experimental autoimmune encephalomyelitis. NLM AIDSLINE Important note: Information in this article was accurate in 1996. The state of the art may have changed since the publication date.

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Lack of requirement for CD8+ cells in recovery from and resistance to experimental autoimmune encephalomyelitis.

J Autoimmun. 1995 Jun;8(3):395-404. Unique Identifier : AIDSLINE MED/96082299
Lohse AW; Schwerdt A; Herkel J; Spahn T; Meyer zum Buschenfelde KH; Department of Medicine, Johannes Gutenberg-University, Mainz,; Germany.

Abstract: Experimental autoimmune encephalomyelitis (EAE) is a model of T-cell mediated autoimmune disease. Active disease is mediated by myelin basic protein specific CD4+ T-cells, whose adoptive transfer can also induce passive disease. In the Lewis rat EAE is a transient disease inducing lasting resistance to rechallenge. The mechanisms of recovery and resistance are poorly understood. CD8+ suppressor T-cells have mostly been thought to be central, especially in resistance to reinduction of the disease. In this study we showed by complete depletion of CD8+ cells that this subset does not influence either recovery or resistance to EAE in the Lewis rat. This was further confirmed by depleting CD8+ cells only after recovery from acute EAE. Such depletion did not diminish the effective resistance to rechallenge. Recovery from and resistance to EAE appear not to require the presence of CD8+ cells.
Keywords: Animal Antibodies, Monoclonal/IMMUNOLOGY/THERAPEUTIC USE CD4-CD8 Ratio CD8-Positive T-Lymphocytes/*IMMUNOLOGY Encephalomyelitis, Allergic/*IMMUNOLOGY/PREVENTION & CONTROL/ THERAPY Female Immunity, Natural Lymphocyte Depletion Rats Rats, Inbred Lew Support, Non-U.S. Gov't JOURNAL ARTICLEKWDanimalantibodies,monoclonal/immunology/therapeuticusecd4-cd8ratiocd8-positivet-lymphocytes/KWDimmunologyencephalomyelitis,allergic/KWDimmunology/prevention&control/therapyfemaleimmunity,naturallymphocytedepletionratsrats,inbredlewsupport,non-uKWDsKWDgov'tjournalarticle
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M9621084

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