The Journal of Experimental Medicine
ThymUS '08
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kang, J.
Right arrow Articles by Raulet, D. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kang, J.
Right arrow Articles by Raulet, D. H.
Right arrowPubmed/NCBI databases
*Gene*GEO Profiles
*HomoloGene*UniGene
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
© 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

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

Correspondence to: David H. Raulet, Department of Molecular and Cell Biology, 485 Life Sciences Addition, University of California at Berkeley, Berkeley, CA 94720. Tel:510-642-9521 Fax:510-642-1443 E-mail:raulet{at}uclink4.berkeley.edu.

Mice lacking the interleukin 7 receptor (IL-7R) generate {alpha}/ß 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}/ß 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


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS