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HLA class II-mediated death is induced via Fas/Fas ligand interactions in
human splenic B lymphocytes
JP Truman, C Choqueux, J Tschopp, J Vedrenne, F Le Deist, D Charron and N Mooney
INSERM U396, Institut Biomedical des Cordeliers, Paris, France.
HLA class II molecules, expressed on the surface of antigen-presenting
cells, are responsible for the presentation of antigen-derived peptides to
CD4+ helper T lymphocytes. Signaling via these molecules initiates the
generation of second messengers leading to programed cell death (PCD) of
activated B lymphocytes. The present study examined the mechanism of HLA
class II-mediated apoptosis and describes the essential role of the
molecule Fas and its ligand (FasL). FasL was expressed in B lymphocytes
after stimulation via HLA class II or with phorbol esters. Expression of
FasL protein was significantly increased in 50% of B lymphocytes after
stimulation via HLA class II, and the level of FasL mRNA was also increased
either by activation with phorbol esters and ionomycin or by signaling via
HLA class II. Although HLA class II signaling did not change the expression
of the Fas molecule, it did lead to increased sensitivity to Fas-mediated
apoptosis. The crucial role of Fas/FasL interactions was confirmed by the
absence of cell death via HLA class II in B cells lacking Fas expression,
and by the significant inhibition of HLA class II-mediated apoptosis in the
presence of either an antagonistic anti-Fas or anti-FasL antibody. These
data demonstrate FasL expression on activated human B lymphocytes and
support the idea that antigen presentation could contribute to the
regulation of lymphocyte populations via Fas and FasL interactions.
Volume 89,
Issue 6,
pp. 1996-2007,
03/15/1997
Copyright © 1997 by The American Society of Hematology
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