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Blood, 30 July 2009, Vol. 114, No. 5, pp. 1026-1028. Prepublished online as a Blood First Edition Paper on May 8, 2009; DOI 10.1182/blood-2009-03-210153. This Article Full Text Full Text (PDF) Supplemental Methods and Figures All Versions of this Article: blood-2009-03-210153v1 114/5/1026    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Google Scholar Articles by Yu, Y. Articles by Yu, X.-Z. PubMed PubMed Citation Articles by Yu, Y. Articles by Yu, X.-Z. Related Collections Immunobiology Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Brief Report Abundant c-Fas–associated death domain–like interleukin-1–converting enzyme inhibitory protein expression determines resistance of T helper 17 cells to activation-induced cell death Yu Yu1, Cristina Iclozan1, Tomohide Yamazaki2, Xuexian Yang2, Claudio Anasetti1,3, Chen Dong2, and Xue-Zhong Yu1,3 1 Departments of Immunology and Blood and Marrow Transplantation, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL; 2 Department of Immunology, M. D. Anderson Cancer Center, Houston, TX; and 3 Department of Oncologic Sciences, University of South Florida, Tampa Activation-induced cell death (AICD) plays an important role in peripheral T-cell tolerance. AICD in CD4 T helper (Th) cells, including Th1 and Th2 effectors, has been extensively studied. Recently, interleukin-17–producing CD4+ T cells (Th17 cells) have been identified as a unique Th subset, but their susceptibility to AICD and the underlying molecular mechanisms have not been defined. In this study, we found that Th17 cells were significantly less susceptible to AICD than Th1 cells, and Th17 cell resistance to AICD is due to the high levels of c-Fas–associated death domain–like interleukin-1–converting enzyme inhibitory protein preventing Fas-mediated apoptosis. The resistance of Th17 cells to AICD reveals a novel mechanism to explain the high pathogenicity of Th17 cells in autoimmune diseases, and may also provide a rationale to generate tumor-specific Th17 cells for adoptive immunotherapy. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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