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CD4+ T cells are required for development of a murine retrovirus- induced immunodeficiency syndrome (MAIDS)

Mice depleted in vivo of CD4+ Th cells by treatment with mAb GK1.5 were found to be resistant to the lymphoproliferative/immunodeficiency disease (MAIDS) induced in intact mice by infection with the mixture of LP-BM5 murine leukemia viruses. Depleted mice did not develop lymphadenopathy or splenomeg...

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Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1988
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2189016/
https://www.ncbi.nlm.nih.gov/pubmed/2842430
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description Mice depleted in vivo of CD4+ Th cells by treatment with mAb GK1.5 were found to be resistant to the lymphoproliferative/immunodeficiency disease (MAIDS) induced in intact mice by infection with the mixture of LP-BM5 murine leukemia viruses. Depleted mice did not develop lymphadenopathy or splenomegaly, had normal serum IgM levels, normal CTL responses to alloantigens, and were able to generate PFC responses to Th-independent antigens even though frequencies of virus-producing spleen cells were comparable in depleted and intact mice. Depletion of CD4+ Th cells after infection resulted in a reversal of many abnormalities exhibited by infected controls; spleen weights, serum IgM levels, and allogeneic CTL responses of treated mice were comparable to those of uninfected controls. These results demonstrate that dysfunction of CD4+ Th cells is central to the induction and progression of both T and B cell abnormalities in MAIDS.
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spelling pubmed-21890162008-04-17 CD4+ T cells are required for development of a murine retrovirus- induced immunodeficiency syndrome (MAIDS) J Exp Med Articles Mice depleted in vivo of CD4+ Th cells by treatment with mAb GK1.5 were found to be resistant to the lymphoproliferative/immunodeficiency disease (MAIDS) induced in intact mice by infection with the mixture of LP-BM5 murine leukemia viruses. Depleted mice did not develop lymphadenopathy or splenomegaly, had normal serum IgM levels, normal CTL responses to alloantigens, and were able to generate PFC responses to Th-independent antigens even though frequencies of virus-producing spleen cells were comparable in depleted and intact mice. Depletion of CD4+ Th cells after infection resulted in a reversal of many abnormalities exhibited by infected controls; spleen weights, serum IgM levels, and allogeneic CTL responses of treated mice were comparable to those of uninfected controls. These results demonstrate that dysfunction of CD4+ Th cells is central to the induction and progression of both T and B cell abnormalities in MAIDS. The Rockefeller University Press 1988-08-01 /pmc/articles/PMC2189016/ /pubmed/2842430 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
CD4+ T cells are required for development of a murine retrovirus- induced immunodeficiency syndrome (MAIDS)
title CD4+ T cells are required for development of a murine retrovirus- induced immunodeficiency syndrome (MAIDS)
title_full CD4+ T cells are required for development of a murine retrovirus- induced immunodeficiency syndrome (MAIDS)
title_fullStr CD4+ T cells are required for development of a murine retrovirus- induced immunodeficiency syndrome (MAIDS)
title_full_unstemmed CD4+ T cells are required for development of a murine retrovirus- induced immunodeficiency syndrome (MAIDS)
title_short CD4+ T cells are required for development of a murine retrovirus- induced immunodeficiency syndrome (MAIDS)
title_sort cd4+ t cells are required for development of a murine retrovirus- induced immunodeficiency syndrome (maids)
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2189016/
https://www.ncbi.nlm.nih.gov/pubmed/2842430