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International Immunology, Vol. 16, No. 3, pp. 501-508, March 2004
© 2004 Japanese Society for Immunology

IL-4-mediated inhibition of IFN-{gamma} production by CD4+ T cells proceeds by several developmentally regulated mechanisms

Olivier Wurtz1, Marc Bajénoff1 and Sylvie Guerder1

1 Centre d’Immunologie de Marseille-Luminy, Institut National de la Santé et de la Recherche Médicale/Centre National de la Recherche Scientifique/Université de la Méditerranée, Parc Scientifique de Luminy, Case 906, 13288 Marseille Cedex 09, France

Correspondence to: S. Guerder; E-mail: guerder{at}ciml.univ-mrs.fr
Transmitting editor: A. Cooke

The mechanisms by which Th1 and Th2 cells inter-regulate in vivo are still poorly understood. In this study we examined the plasticity of Th1 cell differentiation and how Th2 cells may down-regulate these responses. We show here that IL-4 affects Th1 cell responses by two developmentally regulated mechanisms. During the commitment phase of naive CD4+ T cells, IL-4 inhibits Th1 cell differentiation and induces a reversion of developing Th1 cells to the Th2 lineage. In contrast, for effector Th1 cells IL-4 does not affect the developmental process, but only the transcription of the IFN-{gamma} gene. We further show that the difference in IL-4 responsiveness correlates with a loss, in effector Th1 cells, of IL-4-dependent up-regulation of GATA-3 expression despite normal activation of STAT6. Transient inhibition of IFN-{gamma} production by differentiated effector cells may explain why Th1 and Th2 responses can co-exist in vivo although Th2 effector cells dominate functionally, as observed in some infectious or autoimmune mice models.

Keywords: cellular differentiation, gene regulation, Th1/Th2, transcription factor


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