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Blood, 15 August 2005, Vol. 106, No. 4, pp. 1286-1295. Prepublished online as a Blood First Edition Paper on April 21, 2005; DOI 10.1182/blood-2004-10-4074. This Article Full Text (PDF) All Versions of this Article: 2004-10-4074v1 106/4/1286    most recent Alert me when this article is cited Alert me if a correction is posted 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 Tanaka, Y. Articles by Altman, A. Search for Related Content PubMed PubMed Citation Articles by Tanaka, Y. Articles by Altman, A. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted October 26, 2004 Accepted April 6, 2005 Impaired IL-4 and c-Maf expression and enhanced Th1 cell development in Vav1-deficient mice Yoshihiko Tanaka, Takanori So, Svetlana Lebedeva, Michael Croft, and Amnon Altman* Division of Cell Biology, La Jolla Institute for Allergy and Immunology, San Diego, CA, USA Division of Molecular Immunology, La Jolla Institute for Allergy and Immunology, San Diego, CA, USA * Corresponding author; email: amnon{at}liai.org. Although c-Maf is crucial for Th2 differentiation and IL-4 production, its regulation is poorly understood. We report that Vav1-/- CD4+ T cells display deficient TCR/CD28-induced IL-4 and c-Maf expression and, conversely, enhanced IFN production and T-bet expression (even when cultured under Th2-polarizing conditions), but intact expression of other Th2 cytokines and only slightly reduced GATA-3 expression. Upregulation of c-Maf was Ca2+/NFAT-dependent and, together with IL-4 production, could be rescued in Vav1-/- T cells by Ca2+ ionophore. Deficient IL-4 production was restored by retrovirus-mediated Vav1 expression, but only partially by retroviral c-Maf expression. Similar IL-4 IFN skewing was observed in intact, antigen-primed Vav1-/- mice. Thus, Vav1 is selectively required for IL-4 and c-Maf expression, a requirement reflecting, at least in part, the dependence of c-Maf expression on Ca2+/NFAT signaling. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. Charvet, A. J. Canonigo, S. Becart, U. Maurer, A. V. Miletic, W. Swat, M. Deckert, and A. Altman Vav1 Promotes T Cell Cycle Progression by Linking TCR/CD28 Costimulation to FOXO1 and p27kip1 Expression J. Immunol., October 15, 2006; 177(8): 5024 - 5031. [Abstract] [Full Text] [PDF] D. Poppe, I. Tiede, G. Fritz, C. Becker, B. Bartsch, S. Wirtz, D. Strand, S. Tanaka, P. R. Galle, X. R. Bustelo, et al. Azathioprine Suppresses Ezrin-Radixin-Moesin-Dependent T Cell-APC Conjugation through Inhibition of Vav Guanosine Exchange Activity on Rac Proteins J. Immunol., January 1, 2006; 176(1): 640 - 651. [Abstract] [Full Text] [PDF] L. D. Finkelstein, Y. Shimizu, and P. L. Schwartzberg Tec Kinases Regulate TCR-Mediated Recruitment of Signaling Molecules and Integrin-Dependent Cell Adhesion J. Immunol., November 1, 2005; 175(9): 5923 - 5930. [Abstract] [Full Text] [PDF]

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