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ILA, a member of the human nerve growth factor/tumor necrosis factor
receptor family, regulates T-lymphocyte proliferation and survival
H Schwarz, FJ Blanco, J von Kempis, J Valbracht and M Lotz
Sam and Rose Stein Institute for Research on Aging, University of
California at San Diego, La Jolla, CA, USA.
ILA, a gene induced by lymphocyte activation, is a member of the human
nerve growth factor tumor necrosis factor receptor family and the human
homologue of murine 4-1BB. The present study analyzed the role of ILA in
the regulation of human peripheral blood T-lymphocyte function. Antibodies
raised against different fusion proteins recognized ILA on activated
lymphocytes. These antibodies significantly increased anti- CD3--induced
T-lymphocyte proliferation. When anti-CD3--stimulated cells were incubated
on ILA-expressing CHO cells, proliferation was inhibited. CHO cells
transfected with a control construct and not expressing ILA did not reduce
T-cell proliferation. A purified fusion protein containing the
extracellular domain of ILA and the constant domain of human IgG (ILA-IgG)
also inhibited lymphocyte proliferation. Results obtained by 3H-thymidine
incorporation were confirmed by cell cycle analysis that showed a decrease
in the number of lymphocytes in S phase. Lymphocyte morphology in cultures
with ILA-expressing CHO cells was suggestive of apoptosis. Flow cytometry
on propidium iodide-stained cells showed a time-dependent increase in the
number of hypodiploid apoptotic cells when lymphocytes were cultured on
ILA-expressing CHO cells. Internucleosomal DNA cleavage was seen in these
cultures, but not in the presence of ILA-negative CHO cells. Studies on the
mechanism by which ILA regulates T-cell function showed that ILA-IgG
inhibited anti-CD3-induced T-cell proliferation when presented in
immobilized but not in soluble form. These results suggest that ILA may act
by cross- linking its ligand and thereby inhibit T-cell proliferation.
Volume 87,
Issue 7,
pp. 2839-2845,
04/01/1996
Copyright © 1996 by The American Society of Hematology
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