The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1997/1/351/ $5.00
The Journal of Experimental Medicine, Volume 185, Number 2, January 20, 1997 351-356

Brief Definitive Reports

Crucial Role of Jak3 in Negative Selection of Self-reactive T Cells

Kaoru Saijo*, Seung Yong Park*, Yasuo Ishida*,{ddagger}, Hisashi Arase*, and Takashi Saito*

From the * Division of Molecular Genetics, Center for Biomedical Science, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260, {ddagger} Department of Surgical Pathology, Teikyo University School of Medicine, Ichinara Hospital, 3426-3 Anegasaki, Ichihara, Chiba 299-01, Japan

Jak3 mediates growth signals through cytokine receptors such as interleukin-2 (IL-2), IL-4, and IL-7, and its deficiency results in autosomal recessive SCID in mice and humans. In spite of the severely reduced number of lymphocytes in Jak3-deficient mice, the differentiation profile of thymocytes was normal and mature T cells accumulated in the periphery with age. However, we found that self-reactive T cells were not deleted in the thymus and the peripheral tissues in Jak3-deficient mice. All peripheral T cells were in the activation state and thus were unable to be activated further, as demonstrated by the failure of eliciting Ca2+ response upon T cell receptor (TCR) stimulation. From the analysis of TCR-transgenic Jak3-deficient mice, only self-reactive T cells appeared to be in the activated state and anergic. These findings demonstrate a crucial function of Jak3 in the negative selection of autoreactive T cells and the maintenance of functional peripheral T cells.

Address correspondence to Takashi Saito, Division of Molecular Genetics, Center for Biomedical Science, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260, Japan.

This work was supported by grants to T. Saito from the Ministry for Education, Science, and Culture and from the Agency for Science and Technology, Japan and partly by a grant from Ciba-Geigy Foundation (Japan) for the Promotion of Science.


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