Journal
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
Volume 291, Issue 2, Pages G253-G259Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpgi.00409.2005
Keywords
inflammatory bowel disease; helminths; T cells; lamina propria
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Funding
- NIDDK NIH HHS [DK-25295, DK-58755, DK-38327, DK-07663] Funding Source: Medline
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This study determined whether Heligmosomoides polygyrus induces intestinal regulatory T cells. Splenic T cells proliferate strongly when cultured with anti-CD3 and antigen-presenting cells (APC). Lamina propria T cells from mice with H. polygyrus mixed with normal splenic T cells from uninfected mice inhibited proliferation over 90%. Lamina propria T cells from mice without H. polygyrus only modestly affected T cell proliferation. The worm-induced regulatory T cell was CD8(+) and required splenic T cell contact to inhibit proliferation. The regulation also was IL-10 independent, but TAP-dependent, suggesting that it requires major histocompatibility complex (MHC) class I interaction. Additional studies employed mice with transgenic T cells that did not express functional TGF-beta receptors. The lamina propria T regulator inhibited proliferation of these transgenic T cells nearly 100%, suggesting that TGF-beta signaling via the T cell was not required. CD8(+) T cells were needed for worms to reverse piroxicam-induced colitis in Rag mice ( T and B cell deficient) reconstituted with IL-10(-/-) T cells. Thus H. polygyrus induces a regulatory CD8(+) lamina propria T cell that inhibits T cell proliferation and that appears to have a role in control of colitis.
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