HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by King, S. B. S. Articles by Voehringer, D. Search for Related Content PubMed PubMed Citation Articles by King, S. B. S. Articles by Voehringer, D.

Accumulation of Effector CD4 T Cells during Type 2 Immune Responses Is Negatively Regulated by Stat6¹

Institute for Immunology, University of Munich, Munich, Germany

Th2 cells are important effector cells during allergic disorders and parasite infections. Efficient differentiation of Th2 cells requires signaling via the IL-4R and the transcription factor Stat6. Stat6 is further implicated in Th2 cell recruitment to the lung and might be required for the survival of memory Th2 cells. We analyzed the role of Stat6 in T cell expansion, survival, and recruitment to the lung using competitive adoptive transfer experiments and infection with the helminth parasite Nippostrongylus brasiliensis. Stat6 was not required in T cells or other cell types for recruitment of in vivo-generated Th2 cells to the lung. Functional analysis of Th2 memory cells revealed that Stat6 signaling in CD4 T cells was dispensable for memory cell generation, expansion, and cytokine secretion. However, Stat6-deficient T cells survived better than wild-type T cells, resulting in higher accumulation in the bronchoalveolar lavage, lung, and lymph nodes. This demonstrates that effector T cell expansion is negatively controlled by a novel Stat6-dependent mechanism which probably serves to limit the number of effector T cells during the acute phase of the immune response and thereby lowers the risk of bystander toxicity against healthy tissues.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by an Emmy Noether Research Grant from the Deutsche Forschungsgemeinschaft (Vo944/2-2).

² Address correspondence and reprint requests to Dr. David Voehringer, Institute for Immunology, University of Munich, Goethestrasse 31, D-80336 Germany. E-mail address: david.voehringer{at}med.uni-muenchen.de

³ Abbreviations used in this paper: eGFP, enhanced GFP; BAL, bronchoalveolar lavage; FasL, Fas ligand; AICD, activation-induced cell death.

This article has been cited by other articles:

				R. M. Maizels, E. J. Pearce, D. Artis, M. Yazdanbakhsh, and T. A. Wynn Regulation of pathogenesis and immunity in helminth infections J. Exp. Med., September 28, 2009; 206(10): 2059 - 2066. [Abstract] [Full Text] [PDF]

				B. D. Medoff, E. Seung, S. Hong, S. Y. Thomas, B. P. Sandall, J. S. Duffield, D. A. Kuperman, D. J. Erle, and A. D. Luster CD11b+ Myeloid Cells Are the Key Mediators of Th2 Cell Homing into the Airway in Allergic Inflammation J. Immunol., January 1, 2009; 182(1): 623 - 635. [Abstract] [Full Text] [PDF]