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© The Rockefeller University Press, 0022-1007/1999/10/973/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 7, October 4, 1999 973-982

Original Article

Defective Development of {gamma}/{delta} T Cells in Interleukin 7 Receptor–Deficient Mice Is Due to Impaired Expression of T Cell Receptor {gamma} Genes

Joonsoo Kanga, Mark Colesa, and David H. Rauleta

a Department of Molecular and Cell Biology and the Cancer Research Laboratory, Division of Immunology, University of California at Berkeley, Berkeley, California 94720
Department of Molecular and Cell Biology, 485 Life Sciences Addition, University of California at Berkeley, Berkeley, CA 94720.510-642-1443510-642-9521

raulet{at}uclink4.berkeley.edu

Mice lacking the interleukin 7 receptor (IL-7R) generate {alpha}/β T cells at a detectable but greatly reduced rate, but {gamma}/{delta} T cells are completely absent. The special role of IL-7R signaling in {gamma}/{delta} T cell development has remained unclear. IL-7R{alpha}–/– mice exhibit a paucity of {gamma} gene rearrangements. This striking observation can be explained by a defect in T cell receptor (TCR)-{gamma} gene rearrangement, a defect in TCR-{gamma} gene transcription leading to death of {gamma}/{delta} lineage cells, and/or a requirement for IL-7R in commitment of cells to the {gamma}/{delta} lineage. To determine the role of IL-7R signaling in {gamma}/{delta} T cell development, we examined transcription of a prerearranged TCR-{gamma} transgene in IL-7R{alpha}–/– mice, as well as the effects of IL-7 on transcription of endogenous, rearranged TCR-{gamma} genes in {alpha}/β lineage cells. The results demonstrate that IL-7R–mediated signals are necessary for the normal expression of rearranged TCR-{gamma} genes. Equally significant, the results show that the poor expression of TCR-{gamma} genes in IL-7R{alpha}–/– mice is responsible for the selective deficit in {gamma}/{delta} cells in these mice, since a high copy TCR-{gamma} transgene exhibited sufficient residual expression in IL-7R{alpha}–/– mice to drive {gamma}/{delta} cell development. The results indicate that the absence of {gamma}/{delta} T cells in IL-7R{alpha}–/– mice is due to insufficient TCR-{gamma} gene expression.

Key Words: T cell development • interleukin 7 • lineage commitment • T cell receptor gene rearrangement • transcription

1used in this paper: B6, C57BL/6; DN, CD4–CD8– double negative; DP, CD4+CD8+ double positive; HSA, heat-stable antigen; JAK, Janus kinase; RAG, recombination activating gene; RT, reverse transcription; SP, CD4+ or CD8+ single positive; STAT, signal transducer and activator of transcription

M. Coles's present address is Department of Molecular Immunology, National Institute for Medical Research, Mill Hill, London, NW7 1AA, UK.

© 1999 The Rockefeller University Press


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