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1 Microbiology, 2 Neurobiology, University of Alabama, Birmingham, 845 19th St South, BBRB 842, Birmingham, AL, 35294
Abstract
It is well established that CD11a (a.k.a. LFA-1) functions in T cell activation by providing a co-stimulatory signal and by participating in the formation of the immunological synapse. The role of other
2-integrins in T cell activation remains unknown. Recent EAE studies have suggested a role for CD11b and CD11c in T cell biology. These findings prompted us to simultaneously stimulate naïve T cells in vitro, using anti-CD3
and anti-CD11c antibodies. We found that treatment of T cells with anti-CD3
and anti-CD11c (clones N418 or HL3) antibodies substantially suppressed IFN-
production at 72 hours. T cells treated with anti-CD3
and anti-CD11c antibodies do not produce detectable amounts of IL-4 and IL-10 at 12, 24, and 48 hours. In these same cultures, IFN-
production was only detected at 12h post-stimulation, but at a concentration 3 logs lower than that observed with anti-CD3
treatment alone. Interestingly, TGF-
1 production was increased 3 fold on treatment with anti-CD11c and anti-CD3
compared to anti-CD3
treatment alone. The suppression of IL-4, IL-10, and IFN-
production could not be rescued by co-stimulation with anti-CD28 antibodies. Our data suggest that CD11c may be a novel negative regulator in T cell activation.
Supported by NH46032 from the NIH.
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