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B cells are required for induction of T cell abnormalities in a murine retrovirus-induced immunodeficiency syndrome

The role of B cells in induction of phenotypic and functional abnormalities of T cells in a murine retrovirus-induced immunodeficiency syndrome, MAIDS, was evaluated in mice depleted of mature B cells from birth with anti-IgM antibodies (mu-suppressed) and infected at 4 wk of age. Multicolor FACS an...

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Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1990
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187666/
https://www.ncbi.nlm.nih.gov/pubmed/1967300
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description The role of B cells in induction of phenotypic and functional abnormalities of T cells in a murine retrovirus-induced immunodeficiency syndrome, MAIDS, was evaluated in mice depleted of mature B cells from birth with anti-IgM antibodies (mu-suppressed) and infected at 4 wk of age. Multicolor FACS analyses of CD4+ T cell subsets showed that development of phenotypic abnormalities of these cells at 9 wk after infection was completely inhibited by mu- suppression. Furthermore, induction of impaired proliferative responses to Con A and alloantigens and CTL responses to alloantigens was fully blocked in antibody-treated animals. The extent of virus replication was comparable in spleens of untreated and mu-suppressed mice. Retroviral induction of T cell dysfunction in MAIDS is thus dependent on the presence of B cells, and high level virus expression in mice without B cells has little or no effect on T cell function.
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spelling pubmed-21876662008-04-17 B cells are required for induction of T cell abnormalities in a murine retrovirus-induced immunodeficiency syndrome J Exp Med Articles The role of B cells in induction of phenotypic and functional abnormalities of T cells in a murine retrovirus-induced immunodeficiency syndrome, MAIDS, was evaluated in mice depleted of mature B cells from birth with anti-IgM antibodies (mu-suppressed) and infected at 4 wk of age. Multicolor FACS analyses of CD4+ T cell subsets showed that development of phenotypic abnormalities of these cells at 9 wk after infection was completely inhibited by mu- suppression. Furthermore, induction of impaired proliferative responses to Con A and alloantigens and CTL responses to alloantigens was fully blocked in antibody-treated animals. The extent of virus replication was comparable in spleens of untreated and mu-suppressed mice. Retroviral induction of T cell dysfunction in MAIDS is thus dependent on the presence of B cells, and high level virus expression in mice without B cells has little or no effect on T cell function. The Rockefeller University Press 1990-01-01 /pmc/articles/PMC2187666/ /pubmed/1967300 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
B cells are required for induction of T cell abnormalities in a murine retrovirus-induced immunodeficiency syndrome
title B cells are required for induction of T cell abnormalities in a murine retrovirus-induced immunodeficiency syndrome
title_full B cells are required for induction of T cell abnormalities in a murine retrovirus-induced immunodeficiency syndrome
title_fullStr B cells are required for induction of T cell abnormalities in a murine retrovirus-induced immunodeficiency syndrome
title_full_unstemmed B cells are required for induction of T cell abnormalities in a murine retrovirus-induced immunodeficiency syndrome
title_short B cells are required for induction of T cell abnormalities in a murine retrovirus-induced immunodeficiency syndrome
title_sort b cells are required for induction of t cell abnormalities in a murine retrovirus-induced immunodeficiency syndrome
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187666/
https://www.ncbi.nlm.nih.gov/pubmed/1967300