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International Immunology Advance Access originally published online on March 28, 2008
International Immunology 2008 20(6):729-737; doi:10.1093/intimm/dxn031
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© The Japanese Society for Immunology. 2008. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Regulatory role of B-1 B cells in chronic colitis

Yasuyo Shimomura1,2, Emiko Mizoguchi2,3, Ken Sugimoto1,2, Ryoko Kibe4, Yoshimi Benno4, Atsushi Mizoguchi1,2 and Atul K. Bhan1,2

1 Experimental Pathology, Massachusetts General Hospital, Boston, MA 02114, USA
2 Department of Pathology, Harvard Medical School, Boston, MA 02114, USA
3 Gastroenterology Unit, Massachusetts General Hospital, Boston, MA 02114, USA
4 Japan Collection of Microorganisms, RIKEN BioResource Center, Wako, Saitama 310198, Japan

Correspondence to: A. K. Bhan; E-mail: abhan{at}partners.org

According to the ‘hygiene hypothesis’, enhanced microbial exposure due to early childhood infections leads to a reduction of Th2-mediated allergic diseases and inflammatory bowel disease. To begin to elucidate the mechanisms underlying this hypothesis, we studied development of Th2-mediated colitis of the TCR{alpha} knockout (KO) mouse in both a specific pathogen-free (SPF) facility and a conventional (CV) facility. After more than five generations in each facility, TCR{alpha} KO mice kept in the CV facility developed dramatically less colitis than mice that were kept in the SPF facility. Surprisingly, the suppression of colitis in the CV facility correlated with a significant increase in natural IgM production by B-1 B cells. In contrast, B cell-deficient TCR{alpha} double-knockout ({alpha}µ DKO) mice maintained in the CV facility continued to develop severe colitis, strongly suggesting that B-1 B cells contributed to the suppression of colitis. Indeed, the adoptive transfer of B-1 B cells isolated from the peritoneal cavity of TCR{alpha} KO mice (SPF) into {alpha}µ DKO mice (CV) suppressed the development of colitis in the recipient mice. We conclude that B-1 cells play a regulatory role in Th2-mediated colitis under non-hygienic conditions, possibly by generating natural antibodies in response to microbial flora.

Keywords: B-1 B cells, hygiene hypothesis, IBD, KO mice, regulatory B cells, TCR{alpha}

Transmitting editor: C. Terhorst

Received 19 November 2007, accepted 26 February 2008.


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