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International Immunology, Vol. 11, No. 8, 1185-1194, August 1999
© 1999 Japanese Society for Immunology

An alternate pathway for type 1 T cell differentiation

Chiguang Feng, Shohei Watanabe, Saho Maruyama, Gen Suzuki1, Mitsuharu Sato3, Takahisa Furuta2, Somei Kojima2, Shinsuke Taki3 and Yoshihiro Asano

Department of Microbiology and Immunology, Ehime University School of Medicine, Shigenobu, Ehime 791-0295, Japan
1 National Institute of Radiological Science, Chiba 263-8555, Japan
2 >Department of Parasitology, Institute of Medical Science, University of Tokyo, Tokyo 108-0071, Japan
3 >Department of Immunology, Faculty of Medicine, University of Tokyo, Tokyo 113-0033, Japan

Correspondence to: Y. Asano

IFN-regulatory factor-1 (IRF-1) gene-disrupted mice are defective in IL-12 and IL-18 gene expression at the transcriptional and post-translational level respectively. The mutant mouse mounts a type 2 T cell response upon bacterial infection because of the impaired induction of the IL-12 p40 gene and IFN-{gamma}-producing type 1 T cells are not induced. We showed here, however, that different pathogens activate a novel pathway for inducing IFN-{gamma}-producing type 1 T cells even in an IRF-1-deficient mouse. This pathway is independent of IL-12 and IL-18, and is mediated by a distinct function of macrophage lineage cells. Macrophages of the mutant mice fail to activate the IL-12-dependent pathway, but they function in the IL-12-independent pathway in Plasmodium-infected mice. This leads to the hypothesis that the IL-12-independent novel pathway for inducing IFN-{gamma}-producing T cells is distinct from the classical type 1/type 2 T cell subset differentiation pathway.

Keywords: IFN-regulatory factor-1, IL-12, Leishmania major, Listeria monocytogenes, Plasmodium berghei, T cell subsets

Transmitting editor: M. Taniguchi


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