The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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Published online 28 May 2002 doi:10.1084/jem.20011793
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© Rockefeller University Press, 0022-1007/2002/6/1491/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 11, June 3, 2002 1491-1497

Brief Definitive Report

A Unique Subset of Self-specific Intraintestinal T Cells Maintains Gut Integrity

Philippe Poussier1,2,3, Terri Ning1, Diponkar Banerjee4 and Michael Julius1,3

1 Sunnybrook and Women's Health Sciences Centre, University of Toronto, Toronto, Ontario M4N 3M5, Canada
2 Department of Medicine, University of Toronto, Toronto, Ontario M4N 3M5, Canada
3 Department of Immunology, University of Toronto, Toronto, Ontario M4N 3M5, Canada
4 British Columbia Cancer Agency, Vancouver, British Columbia Y5Z4E6, Canada

Address correspondence to Philippe Poussier, Sunnybrook and Women's Health Sciences Centre, 2075 Bayview Ave., Room A3 38, Toronto, Ontario M4N 3M5, Canada. Phone: 416-480-6136; Fax: 416-480-4375; E-mail: ppoussie{at}sten.sunnybrook.utoronto.ca

Lymphocytes residing in the intestinal epithelium are exclusively T cells and account for one of the largest collection of T cells in the organism. However, their function remains obscure. We and others have shown that the development of intestinal intraepithelial T cells is compromised in mutant mice prone to chronic intestinal inflammation. These results led us to directly assess their role in regulating the development of colitis secondary to transfer of primary splenic TCR{alpha}ß+CD4+CD45RBhi T cells into severe combined immunodeficiency (SCID) mice. Here we demonstrate that prior reconstitution of SCID recipients with intraintestinal TCR{alpha}ß+CD4-CD8{alpha}+ß- T cells prevents disease, and does so in an interleukin (IL)-10–dependent fashion. In contrast, reconstitution with either TCR{gamma}{delta}+ or TCR{alpha}ß+CD4- CD8{alpha}+ß+ intestinal T cells did not prevent colitis. TCR{alpha}ß+CD4-8{alpha}+ß- T cells are unique to the intestinal epithelium of both rodents and humans. Previous repertoire analyses of TCR{alpha}ß+CD4-CD8{alpha}+ß- T cells revealed a high proportion of cells expressing high affinity, self-specific TCR within this subset. We demonstrate that monoclonal, self specific TCR{alpha}ß+CD4-CD8{alpha}+ß- cells derived from TCR transgenic mice also prevent the onset of colitis. Thus, intestinal TCR{alpha}ß+CD4-CD8{alpha}+ß- T cells, selected based on their self-reactivity, maintain gut integrity in a IL-10–dependent fashion.

Key Words: regulatory • autoreactive • TCR{alpha}ß+CD4-CD8{alpha}+ß- IEL • IL-10 • IBD


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