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Cytokine-induced immune deviation as a therapy for inflammatory autoimmune disease

The properties and outcome of an immune response are best predicted by the lymphokine phenotype of the responding T cells. Cytokines produced by CD4+ T helper type 1 (Th1) T cells mediate delayed type hypersensitivity (DTH) and inflammatory responses, whereas cytokines produced by Th2 T cells mediat...

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Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1994
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2191757/
https://www.ncbi.nlm.nih.gov/pubmed/7525845
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description The properties and outcome of an immune response are best predicted by the lymphokine phenotype of the responding T cells. Cytokines produced by CD4+ T helper type 1 (Th1) T cells mediate delayed type hypersensitivity (DTH) and inflammatory responses, whereas cytokines produced by Th2 T cells mediate helper T cell functions for antibody production. To determine whether induction of Th2-like cells would modulate an inflammatory response, interleukin 4 (IL-4) was administered to animals with experimental allergic encephalomyelitis (EAE), a prototypic autoimmune disease produced by Th1-like T cells specific for myelin basic protein (MBP). IL-4 treatment resulted in amelioration of clinical disease, the induction of MBP-specific Th2 cells, diminished demyelination, and inhibition of the synthesis of inflammatory cytokines in the central nervous system (CNS). Modulation of an immune response from one dominated by excessive activity of Th1- like T cells to one dominated by the protective cytokines produced by Th2-like T cells may have applicability to the therapy of certain human autoimmune diseases.
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spelling pubmed-21917572008-04-16 Cytokine-induced immune deviation as a therapy for inflammatory autoimmune disease J Exp Med Articles The properties and outcome of an immune response are best predicted by the lymphokine phenotype of the responding T cells. Cytokines produced by CD4+ T helper type 1 (Th1) T cells mediate delayed type hypersensitivity (DTH) and inflammatory responses, whereas cytokines produced by Th2 T cells mediate helper T cell functions for antibody production. To determine whether induction of Th2-like cells would modulate an inflammatory response, interleukin 4 (IL-4) was administered to animals with experimental allergic encephalomyelitis (EAE), a prototypic autoimmune disease produced by Th1-like T cells specific for myelin basic protein (MBP). IL-4 treatment resulted in amelioration of clinical disease, the induction of MBP-specific Th2 cells, diminished demyelination, and inhibition of the synthesis of inflammatory cytokines in the central nervous system (CNS). Modulation of an immune response from one dominated by excessive activity of Th1- like T cells to one dominated by the protective cytokines produced by Th2-like T cells may have applicability to the therapy of certain human autoimmune diseases. The Rockefeller University Press 1994-11-01 /pmc/articles/PMC2191757/ /pubmed/7525845 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Articles
Cytokine-induced immune deviation as a therapy for inflammatory autoimmune disease
title Cytokine-induced immune deviation as a therapy for inflammatory autoimmune disease
title_full Cytokine-induced immune deviation as a therapy for inflammatory autoimmune disease
title_fullStr Cytokine-induced immune deviation as a therapy for inflammatory autoimmune disease
title_full_unstemmed Cytokine-induced immune deviation as a therapy for inflammatory autoimmune disease
title_short Cytokine-induced immune deviation as a therapy for inflammatory autoimmune disease
title_sort cytokine-induced immune deviation as a therapy for inflammatory autoimmune disease
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2191757/
https://www.ncbi.nlm.nih.gov/pubmed/7525845