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Departments of
*
Neurology and
Microbiology and Molecular Immunology, University of Southern California School of Medicine, Los Angeles, CA 90033
CD8+ effectors are critical components of type 1
responses against viral infections as well as for antiviral vaccines.
IL-4 plays a clear role as an inhibitor of CD4+ Th1 cells;
however, its role in CD8+ T cell regulation appears to be
more complex. Thus, IL-4 may augment CD8+ T cell growth,
but also limit effector function. Moreover, abundant IL-4 is inhibitory
for viral clearance, but the lack of IL-4 appears not to affect
CTL-mediated immunity. This report investigates these disparate roles
of IL-4 in CD8+ T lymphocyte regulation by comparing T cell
responses specific for a single HIV-IIIIB gp120-derived
epitope in BALB/c mice deficient in IL-4 to those in wild-type
controls. CTL activation was monitored during the acute and memory
phases following immunization with recombinant vaccinia virus. Similar
frequencies of gp120-specific CTL precursors in splenocytes from both
groups indicated that IL-4 plays no significant role in either CTL
priming or the establishment of memory. However, cytolytic activity in
cultures derived from IL-4-deficient mice developed earlier and was
strikingly enhanced following in vitro restimulation, an effect
exhibited by both primary and memory T cells. Secretion of IL-2 and
IFN-
by CD8+ T cells from IL-4-deficient mice was also
elevated, reflecting their enhanced activation. Thus, IL-4 appears to
limit the activation, expansion, and differentiation of
CD8+ T cells with high cytolytic
potential.
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