T-B cell interaction inhibits spontaneous apoptosis of mature lymphocytes in Bcl-2-deficient mice

Bcl-2 expression is tightly regulated during lymphocyte development. Mature lymphocytes in Bcl-2-deficient mice show accelerated spontaneous apoptosis in vivo and in vitro. Stimulation of Bcl-2-deficient lymphocytes by anti-CD3 antibody inhibited the spontaneous apoptosis not only in T cells but als...

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Formato: Online Artículo Texto
Lenguaje:inglés
Publicado: The Rockefeller University Press 1995
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192300/
https://www.ncbi.nlm.nih.gov/pubmed/7561683
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collection PubMed
description Bcl-2 expression is tightly regulated during lymphocyte development. Mature lymphocytes in Bcl-2-deficient mice show accelerated spontaneous apoptosis in vivo and in vitro. Stimulation of Bcl-2-deficient lymphocytes by anti-CD3 antibody inhibited the spontaneous apoptosis not only in T cells but also in B cells. The rescue of B cells was dependent on the presence of T cells, mainly through CD40L and interleukin (IL)-4. Furthermore, we generated Bcl-2-deficient mice transgenic for a T cell receptor or an immunoglobulin, both specific for chicken ovalbumin, to test for antigen-specific T-B cell interaction in the inhibition of the spontaneous apoptosis. The initial T cell activation by antigenic peptides presented by B cells suppressed apoptosis in T cells. Subsequently, T cells expressed CD40L and released ILs, leading to the protection of B cells from spontaneous apoptosis. These results suggest that the antiapoptotic signaling via CD40 or IL-4 may be largely independent of Bcl-2. Engagement of the Ig alone was not sufficient for the inhibition of B cell apoptosis. Thus, the physiological role of Bcl-2 in mature lymphocytes may be to protect cells from spontaneous apoptosis and to extend their lifespans to increase the opportunity for T cells and B cells to interact with each other and specific antigens in secondary lymphoid tissues. Bcl-2, however, appears to be dispensable for survival once mature lymphocytes are activated by antigen-specific T-B cell collaboration.
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spelling pubmed-21923002008-04-16 T-B cell interaction inhibits spontaneous apoptosis of mature lymphocytes in Bcl-2-deficient mice J Exp Med Articles Bcl-2 expression is tightly regulated during lymphocyte development. Mature lymphocytes in Bcl-2-deficient mice show accelerated spontaneous apoptosis in vivo and in vitro. Stimulation of Bcl-2-deficient lymphocytes by anti-CD3 antibody inhibited the spontaneous apoptosis not only in T cells but also in B cells. The rescue of B cells was dependent on the presence of T cells, mainly through CD40L and interleukin (IL)-4. Furthermore, we generated Bcl-2-deficient mice transgenic for a T cell receptor or an immunoglobulin, both specific for chicken ovalbumin, to test for antigen-specific T-B cell interaction in the inhibition of the spontaneous apoptosis. The initial T cell activation by antigenic peptides presented by B cells suppressed apoptosis in T cells. Subsequently, T cells expressed CD40L and released ILs, leading to the protection of B cells from spontaneous apoptosis. These results suggest that the antiapoptotic signaling via CD40 or IL-4 may be largely independent of Bcl-2. Engagement of the Ig alone was not sufficient for the inhibition of B cell apoptosis. Thus, the physiological role of Bcl-2 in mature lymphocytes may be to protect cells from spontaneous apoptosis and to extend their lifespans to increase the opportunity for T cells and B cells to interact with each other and specific antigens in secondary lymphoid tissues. Bcl-2, however, appears to be dispensable for survival once mature lymphocytes are activated by antigen-specific T-B cell collaboration. The Rockefeller University Press 1995-10-01 /pmc/articles/PMC2192300/ /pubmed/7561683 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
T-B cell interaction inhibits spontaneous apoptosis of mature lymphocytes in Bcl-2-deficient mice
title T-B cell interaction inhibits spontaneous apoptosis of mature lymphocytes in Bcl-2-deficient mice
title_full T-B cell interaction inhibits spontaneous apoptosis of mature lymphocytes in Bcl-2-deficient mice
title_fullStr T-B cell interaction inhibits spontaneous apoptosis of mature lymphocytes in Bcl-2-deficient mice
title_full_unstemmed T-B cell interaction inhibits spontaneous apoptosis of mature lymphocytes in Bcl-2-deficient mice
title_short T-B cell interaction inhibits spontaneous apoptosis of mature lymphocytes in Bcl-2-deficient mice
title_sort t-b cell interaction inhibits spontaneous apoptosis of mature lymphocytes in bcl-2-deficient mice
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192300/
https://www.ncbi.nlm.nih.gov/pubmed/7561683