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Department of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia, Canada
T cell activation requires a threshold amount of TCR-mediated
signals, an amount that is reduced by signals mediated through
costimulatory molecules expressed on the T cell surface. Here the role
of TNFR2 (p75) as a putative costimulatory receptor for T cell
activation was examined. It was found that p75 deficiency in
CD8+ T cells increased the requirements for TCR agonist
approximately 5-fold. Furthermore, p75-/- T cells display
a marked reduction in the proliferative response to TCR agonist. This
hypoproliferative response was associated with delayed kinetics of
induction of the acute activation markers CD25 and CD69 as well as a
marked decrease in the production of IL-2 and IFN-
. The net result
is that very few cells are recruited into the dividing population.
Interestingly, CD28 costimulation was only partially effective in
rescuing the proliferative defect of
p75-/-CD8+ T cells. Thus, p75 provides an
important costimulatory signal in addition to that provided by CD28
toward optimal T cell proliferation.
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