Induction and regulation of inflammatory bowel disease in immunodeficient mice by distinct CD4+ T-cell subsets.

Although the etiology of human inflammatory bowel disease (IBD) has not yet been completely defined, the current prevailing hypothesis is that it is caused by aberrant immune responses, or loss of tolerance, toward components of the intestinal bacterial microflora. During the past decade, several an...

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Автор: Maloy, K
Формат: Journal article
Мова:English
Опубліковано: 2007
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author Maloy, K
author_facet Maloy, K
author_sort Maloy, K
collection OXFORD
description Although the etiology of human inflammatory bowel disease (IBD) has not yet been completely defined, the current prevailing hypothesis is that it is caused by aberrant immune responses, or loss of tolerance, toward components of the intestinal bacterial microflora. During the past decade, several animal models of IBD have been developed that reproduce many features of the human disease. This article will outline one of the best characterized murine IBD models, the "T-cell transfer model" where colitis rapidly develops following adoptive transfer of naive CD4+CD45RB high T cells into immunodeficient scid or RAG-/- mice. This model has also been instrumental in characterizing the potent suppressive activities of CD4+CD25+ regulatory T cells that prevent the development of IBD when cotransferred with the naive CD4+ T cells. The T cell transfer model of IBD is reproducible and easily manipulated and therefore provides an excellent system for the study of immunopathology and immune regulation in the intestine.
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spelling oxford-uuid:fe491ada-8ff7-4de0-a19e-259a79eb7b322022-03-27T13:35:13ZInduction and regulation of inflammatory bowel disease in immunodeficient mice by distinct CD4+ T-cell subsets.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:fe491ada-8ff7-4de0-a19e-259a79eb7b32EnglishSymplectic Elements at Oxford2007Maloy, KAlthough the etiology of human inflammatory bowel disease (IBD) has not yet been completely defined, the current prevailing hypothesis is that it is caused by aberrant immune responses, or loss of tolerance, toward components of the intestinal bacterial microflora. During the past decade, several animal models of IBD have been developed that reproduce many features of the human disease. This article will outline one of the best characterized murine IBD models, the "T-cell transfer model" where colitis rapidly develops following adoptive transfer of naive CD4+CD45RB high T cells into immunodeficient scid or RAG-/- mice. This model has also been instrumental in characterizing the potent suppressive activities of CD4+CD25+ regulatory T cells that prevent the development of IBD when cotransferred with the naive CD4+ T cells. The T cell transfer model of IBD is reproducible and easily manipulated and therefore provides an excellent system for the study of immunopathology and immune regulation in the intestine.
spellingShingle Maloy, K
Induction and regulation of inflammatory bowel disease in immunodeficient mice by distinct CD4+ T-cell subsets.
title Induction and regulation of inflammatory bowel disease in immunodeficient mice by distinct CD4+ T-cell subsets.
title_full Induction and regulation of inflammatory bowel disease in immunodeficient mice by distinct CD4+ T-cell subsets.
title_fullStr Induction and regulation of inflammatory bowel disease in immunodeficient mice by distinct CD4+ T-cell subsets.
title_full_unstemmed Induction and regulation of inflammatory bowel disease in immunodeficient mice by distinct CD4+ T-cell subsets.
title_short Induction and regulation of inflammatory bowel disease in immunodeficient mice by distinct CD4+ T-cell subsets.
title_sort induction and regulation of inflammatory bowel disease in immunodeficient mice by distinct cd4 t cell subsets
work_keys_str_mv AT maloyk inductionandregulationofinflammatoryboweldiseaseinimmunodeficientmicebydistinctcd4tcellsubsets