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1
*
Department of Medical Microbiology, Windeyer Institute of Medical Sciences, Royal Free and University College Medical School, London, United Kingdom; and
Department of Microbiology, National University of Singapore, Singapore
T cell apoptosis is associated with defective cell-mediated
effector functions in several infectious diseases. In tuberculosis,
there is evidence that T cell apoptosis may be cytokine mediated, but
the mechanisms are not clearly understood. Type 2 cytokines have
recently been associated with disease extent in human tuberculosis, but
they have not previously been linked to apoptosis in
mycobacterium-reactive T cells. This study presents evidence that PBLs
from healthy donors respond to sonicated Mycobacterium
tuberculosis Ags with increased IL-4 gene activation, CD30
expression, and apoptosis. The changes were significantly greater than
those observed when cells were stimulated with Ags from nonpathogenic
Mycobacterium vaccae. A hypothesis linking these
observations was tested. CD30 expression and TNF-
-mediated
lymphocyte apoptosis were both down-regulated by inhibiting IL-4 in
this model. TNFR-associated factor 2 (TRAF2) expression was
down-regulated in CD30+ cells, and addition of
anti-TNF- Ab significantly reduced apoptosis in the
CD30+ but not the CD30- population. These
observations support the hypothesis that increased IL-4 expression in
M. tuberculosis-activated lymphocytes promotes CD30
expression, which sensitizes the lymphocytes to TNF--mediated
apoptosis via TRAF2 depletion. This may be one mechanism by which IL-4
is associated with immunopathological consequences in human
tuberculosis.
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