The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1996/12/2423/ $5.00
The Journal of Experimental Medicine, Volume 184, Number 6, December 1, 1996 2423-2428

Brief Definitive Reports

The V–J Recombination of T Cell Receptor-{gamma} Genes Is Blocked in Interleukin-7 Receptor–deficient Mice

Kazushige Maki*, Shinji Sunaga*, and Koichi Ikuta*,{ddagger}

From the * Department of Disease-related Gene Regulation Research (Sandoz), Faculty of Medicine, The University of Tokyo, Tokyo 113, Japan; and the {ddagger} Department of Medical Chemistry, Faculty of Medicine, Kyoto University, Kyoto 606, Japan

IL-7R-deficient mice have severely impaired expansion of early lymphocytes and lack {gamma}{delta} T cells. To elucidate the role of IL-7R on {gamma}{delta} T cell development, we analyzed the rearrangements of TCR-{alpha}, β, {gamma}, and {delta} genes in the thymus of the IL-7R-deficient mice. Southern blot analysis with a J{gamma}1 probe revealed that more than 70% of J{gamma}1 and J{gamma}2 alleles are recombined to form distinct V{gamma}1.2–J{gamma}2 and V{gamma}2–J{gamma}1 fragments in control mice. On the contrary, no such recombination was detected in the mutant mice. The rearrangements in the TCR-{alpha}, β, and {delta} loci were comparably observed in control and mutant mice. PCR analysis indicated that the V–J recombination of all the V{gamma} genes is severely hampered in the mutant mice. The mRNA of RAG-1, RAG-2, Ku-80, and terminal deoxynucleotidyl transferase (TdT) genes was equally detected between control and mutant thymi, suggesting that the expression of common recombination machinery is not affected. These data demonstrated that the V–J recombination of the TCR {gamma} genes is specifically blocked in the IL-7R-deficient mice and suggested the presence of highly specific regulation for TCR {gamma} gene rearrangement.

Address correspondence to Koichi Ikuta, Department of Medical Chemistry, Faculty of Medicine, Kyoto University, Yoshida, Sakyo-ku, Kyoto 606, Japan.

This work was supported by a grant-in-aid from the Ministry of Education, Science, and Culture of Japan, and by the grant provided by the Ichiro Kanehara Foundation.


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