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The Journal of Immunology, 2007, 178: 88.6.
Copyright © 2007 by The American Association of Immunologists, Inc.

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88.6

CD11c is Critical in Modulating Cytokine Production by Activated T cells

Jillian E Adams1 and Scott Barnum1,2

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 beta2-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{varepsilon} and anti-CD11c antibodies. We found that treatment of T cells with anti-CD3{varepsilon} and anti-CD11c (clones N418 or HL3) antibodies substantially suppressed IFN-{gamma} production at 72 hours. T cells treated with anti-CD3{varepsilon} 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-{gamma} production was only detected at 12h post-stimulation, but at a concentration 3 logs lower than that observed with anti-CD3{varepsilon} treatment alone. Interestingly, TGF-beta1 production was increased 3 fold on treatment with anti-CD11c and anti-CD3{varepsilon} compared to anti-CD3{varepsilon} treatment alone. The suppression of IL-4, IL-10, and IFN-{gamma} 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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