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Interleukin‐10 rescues T cells from apoptotic cell death: association with an upregulation of Bcl‐2
Author(s) -
COHEN S. B. A.,
CRAWLEY J. B.,
KAHAN M. C.,
FELDMANN M.,
FOXWELL B. M. J.
Publication year - 1997
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1997.00348.x
Subject(s) - downregulation and upregulation , apoptosis , programmed cell death , association (psychology) , cancer research , microbiology and biotechnology , biology , genetics , psychology , gene , psychotherapist
We demonstrate that interleukin‐10 (IL‐10) can inhibit T‐cell apoptosis. T cells, within a PBMC (peripheral blood mononuclear cell) population, were stimulated via the T‐cell receptor and grown in the presence of IL‐2. These cells had less apoptosis when in the continuous presence of IL‐10, compared with cells grown in the absence of IL–10. Conversely, when stimulated and grown in the presence of neutralizing antibody to IL‐10, there was an increase in T‐cell apoptosis. The in vitro rescue from apoptotic cell death of other lymphoid cells, such as germinal centre B cells, has been shown by others to involve a Bcl‐2 pathway. We therefore investigated whether IL‐10 might affect the Bcl‐2 expression on cultured T cells. By Western blotting we demonstrated that continuous exposure of IL‐10 to T cells (within a PBMC population) enhanced the expression of Bcl‐2. Furthermore, T cells protected from apoptotic cell death by IL‐10 were indistinguishable from viable untreated cells in their ability to proliferate to either immobilized anti‐CD3 or IL‐2. Thus, we have shown that continuous culture of T cells in the presence of IL‐10 will inhibit T‐cell apoptosis because of, at least in part, the upregulation of Bcl‐2, and this is associated with a normal proliferative function.