AJP - GI Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Gastrointest Liver Physiol 285: G382-G388, 2003. First published April 17, 2003; doi:10.1152/ajpgi.00373.2002
0193-1857/03 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
285/2/G382    most recent
00373.2002v2
00373.2002v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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 Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Boone, D. L.
Right arrow Articles by Ma, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Boone, D. L.
Right arrow Articles by Ma, A.

INFLAMMATION/IMMUNITY/MEDIATORS

Fas is not essential for lamina propria T lymphocyte homeostasis

David L. Boone,* Themistocles Dassopoulos,* Sophia Chai, Marcia Chien, James Lodolce, and Averil Ma

Department of Medicine, Inflammatory Bowel Disease Research Center and Committee on Immunology, The University of Chicago, Chicago, Illinois 60637

Submitted 30 August 2002 ; accepted in final form 9 April 2003

IL-2 receptor {alpha}-deficient (IL2R{alpha}-/-) mice spontaneously accumulate vast numbers of intestinal lamina propria (LP) T cells and develop bowel inflammation. The accumulation of T cells in IL2R{alpha}-/- mice is thought to result, in part, from defective Fas-induced cell death. To understand the role of cell proliferation and death in regulating LP T cells in IL2R{alpha}-/- mice, we have directly examined the proliferation and Fas sensitivity of wild-type, lpr/lpr, and IL2R{alpha}-/- LP T cells. In wild-type mice, 5'-bromodeoxyuridine (BrdU) labeling and Fas susceptibility are greatest in CD44Hi LP T cells. Fas-deficient lpr/lpr mice have normal total numbers of LP T cells, despite an increased proportion of BrdU+ T cells. By contrast, IL2R{alpha}-/- mice possess increased total numbers of LP T cells, despite normal proportions of BrdU+ LP T cells. Finally, wild-type and IL2R{alpha}-/- LP T cells are equivalently Fas sensitive. These results demonstrate that LP T cells proliferate and are Fas-sensitive cells. IL2R{alpha}-/- mice accumulate a large number of these Fas-sensitive LP T cells and clearly differ from Fas-deficient lpr/lpr mice in this regard. Thus our studies reveal that Fas is dispensable for LP T cell homeostasis and suggest that the intestinal inflammation observed in IL2R{alpha}-/- mice is independent of defective Fas-induced cell death.

intestinal inflammation; colitis


Address for reprint requests and other correspondence: A. Ma, Univ. of Chicago, Medicine Dept., Committee on Immunology, MC 6084, 5841 S. Maryland Ave., Chicago, IL 60637 (E-mail: ama{at}medicine.bsd.uchicago.edu).






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2003 by the American Physiological Society.