Skip Navigation


International Immunology Advance Access originally published online on January 31, 2005
International Immunology 2005 17(3):233-243; doi:10.1093/intimm/dxh204
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
17/3/233    most recent
dxh204v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (8)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Zhang, Y.
Right arrow Articles by Wu, M. X.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhang, Y.
Right arrow Articles by Wu, M. X.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© The Japanese Society for Immunology. 2005. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org

Accelerated transition from the double-positive to single-positive thymocytes in G{alpha}i2-deficient mice

Yujin Zhang1, Milton J. Finegold1, YongZhu Jin2 and Mei X. Wu1,2

1 Department of Pathology, Baylor College of Medicine, Houston, TX 77030, USA
2 Wellman Center of Photomedicine, Massachusetts General Hospital and Department of Dermatology, Harvard Medical School, Boston, MA 02114, USA

Correspondence to: M. X. Wu; E-mail: mwu2{at}partners.org

Deletion of {alpha}i2 subunit of heterotrimeric G proteins induces a 2–4-fold increase in the proportions of CD4 and CD8 single-positive (SP) thymocytes as compared with wild-type littermates, but how G{alpha}i2 is involved in thymocyte development is unknown. To determine a role for G{alpha}i2 in a specific developmental stage of thymocyte differentiation, we studied the ontogeny of thymocytes in G{alpha}i2-deficient mice. Our data show that an accelerated transition from the double-positive (DP) to SP thymocytes, rather than impairment in thymic emigration, accounts for a high proportion of the SP thymocytes in the absence of G{alpha}i2. Lack of G{alpha}i2 greatly augmented a response of thymocytes to TCR-mediated stimulation, as evidenced by enhanced proliferation of the DP thymocytes upon ligation of the TCRs. The augmented response may be the reason behind the expedited transition from the DP to SP thymocytes in the animal. In accordance with this, effects of G{alpha}i2 deficiency on CD8 or CD4 SP thymocyte differentiation required engagement of the TCRs with either MHC class I or MHC class II molecule. The abnormal thymocyte development resulted in an increase in positive selection, altered usage of TCR Vß gene, aberrant development of CD4+CD25+ T regulatory cells and untimely thymic involution, the contribution of which to colitis development in the animal is discussed. These findings reveal a previously unappreciated role for G{alpha}i2 protein in clonal selection and functionality of thymocytes.

Keywords: colitis, Gai2, positive selection, TCR

Transmitting editor: T. Tedder.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Hum ReprodHome page
K. S. Monkkonen, R. Aflatoonian, K.-F. Lee, W. S.B. Yeung, S.-W. Tsao, J. T. Laitinen, E. M. Tuckerman, T.C. Li, and A. Fazeli
Localization and variable expression of G{alpha}i2 in human endometrium and Fallopian tubes
Hum. Reprod., May 1, 2007; 22(5): 1224 - 1230.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
B. D. Thompson, Y. Jin, K. H. Wu, R. A. Colvin, A. D. Luster, L. Birnbaumer, and M. X. Wu
Inhibition of G{alpha}i2 Activation by G{alpha}i3 in CXCR3-mediated Signaling
J. Biol. Chem., March 30, 2007; 282(13): 9547 - 9555.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.