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Blood, 15 January 2007, Vol. 109, No. 2, pp. 449-456. Prepublished online as a Blood First Edition Paper on September 14, 2006; DOI 10.1182/blood-2006-04-018101. This Article Full Text Full Text (PDF) Supplemental Figure All Versions of this Article: blood-2006-04-018101v1 109/2/449    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 HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Yasuda, T. Articles by Kakiuchi, T. Search for Related Content PubMed PubMed Citation Articles by Yasuda, T. Articles by Kakiuchi, T. Related Collections Immunobiology Apoptosis Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CHEMOKINES, CYTOKINES, AND INTERLEUKINS Chemokines CCL19 and CCL21 promote activation-induced cell death of antigen-responding T cells Takuwa Yasuda1,2, Taku Kuwabara1, Hideki Nakano1, Kentaro Aritomi1,3, Takashi Onodera2, Martin Lipp4, Yousuke Takahama5, and Terutaka Kakiuchi1, 1 Department of Immunology, Toho University School of Medicine, Tokyo, Japan; 2 Department of Molecular Immunology, Graduate School of Agriculture and Life Sciences, University of Tokyo, Japan; 3 Department of Orthopedic Surgery, Juntendo University School of Medicine, Tokyo, Japan; 4 Department of Molecular Tumorgenetics and Immunogenetics, Max-Delbrück Center for Molecular Medicine, Berlin, Germany; 5 Division of Experimental Immunology, Institute for Genome Research, University of Tokushima, Japan Secondary lymphoid organs (SLOs) provide a niche for the initiation and regulation of T-cell responses, but the mechanisms have been poorly understood. We investigated the influence of chemokines CCL19 and CCL21 constitutively expressed in SLOs on activation-induced cell death (AICD) of CD4+ T cells. When paucity of lymph node T cells (plt) mutant mice lacking expression of CCL19/CCL21 were primed with OVA/CFA, both expansion of OVA-responding CD4+ T cells in the draining lymph nodes and an in vitro recall response were prolonged as compared with responses in wild-type (WT) mice. The apoptotic cell frequency among OVA-responding CD4+ T cells was similarly low in plt/plt and WT mice during the clonal expansion phase. However, during the clonal contraction phase, the frequency never increased in plt/plt mice, whereas in WT mice it continuously increased to a peak 18 days after immunization. The presence of CCL19/CCL21 during the in vitro stimulation of CD4+ T cells with anti-CD3 plus anti-CD28 significantly enhanced in vitro AICD induction of the restimulated T cells, partially through enhancing expression of Fas ligand. Our results suggest that CCL19/CCL21 produced by stromal cells and antigen-presenting cells regulate CD4+ T-cell immune responses in SLOs by promoting AICD. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Kuwabara, F. Ishikawa, T. Yasuda, K. Aritomi, H. Nakano, Y. Tanaka, Y. Okada, M. Lipp, and T. Kakiuchi CCR 7 Ligands Are Required for Development of Experimental Autoimmune Encephalomyelitis through Generating IL-23-Dependent Th17 Cells J. Immunol., August 15, 2009; 183(4): 2513 - 2521. [Abstract] [Full Text] [PDF] A. C. M. Davalos-Misslitz, T. Worbs, S. Willenzon, G. Bernhardt, and R. Forster Impaired responsiveness to T-cell receptor stimulation and defective negative selection of thymocytes in CCR7-deficient mice Blood, December 15, 2007; 110(13): 4351 - 4359. [Abstract] [Full Text] [PDF]

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