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Blood, 19 March 2009, Vol. 113, No. 12, pp. 2684-2694. Prepublished online as a Blood First Edition Paper on January 9, 2009; DOI 10.1182/blood-2008-05-157966. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2008-05-157966v1 113/12/2684    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 Citing Articles via Google Scholar Google Scholar Articles by Miwa, T. Articles by Song, W.-C. Search for Related Content PubMed PubMed Citation Articles by Miwa, T. Articles by Song, W.-C. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Complement-dependent T-cell lymphopenia caused by thymocyte deletion of the membrane complement regulator Crry Takashi Miwa1, Lin Zhou1, Yuko Kimura1, David Kim1, Avinash Bhandoola2, and Wen-Chao Song1 1 Institute for Translational Medicine and Therapeutics and Department of Pharmacology, and 2 Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia Although complement lysis is frequently used for the purification of lymphocyte subpopulations in vitro, how lymphocytes escape complement attack in vivo has not been clearly delineated. Here, we show that conditional gene targeting of a murine membrane complement regulator Crry on thymocytes led to complement-dependent peripheral T-cell lymphopenia. Notably, despite evidence of hypersensitivity to complement attack, Crry-deficient T cells escaped complement injury and developed normally in the thymus, because of low intrathymic complement activity. Crry-deficient T cells were eliminated in the periphery by a C3- and macrophage-mediated but C5-independent mechanism. Thus, Crry is essential for mature T-cell survival in the periphery but not for lymphogenesis in the thymus. The observation that the thymus is a complement-privileged site may have implications for complement-based antitumor therapies. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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