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A more recent version of this article appeared on May 1, 2007

Published online before print February 20, 2007
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0306218

Received for publication March 23, 2006.
Revised December 15, 2006.
Accepted for publication January 18, 2007.

Article

Contrasting effects of FLIPL overexpression in human T cells on activation-induced cell death and cytokine production

Jehad Charo @ and Paul F. Robbins

Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA

@ To whom correspondence should be addressed. E-mail: j.charo{at}mdc-berlin.de.


  Abstract

There have been disparate findings about the role of FLIP in the survival of mouse T cells and human tumor cell lines. The role of cellular FLIP in human T cell activation and function needs to be clarified further. To study this role, we have overexpressed long transcript FLIP (FLIPL) in primary T cells, including self-antigen-reactive, melanoma-specific T cells. We found that FLIPL overexpression protects human T cells from activation-induced cell death and enhances their prolifertive capacity but suppresses the ability of these cells to produce the proinflammatory cytokines IL-2 and IFN-{gamma} in response to CD3 or antigen-specific stimulation. The multiple effects of FLIPL indicate that this protein may influence T cell responses to antigenic stimulation.

Key Words: tumor • autoimmunity • apoptosis • cellular activation • tolerance






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