Skip Navigation



International Immunology Advance Access published online on March 28, 2008
International Immunology, doi:10.1093/intimm/dxn031
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
20/6/729    most recent
dxn031v1
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 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 arrowRequest Permissions
Google Scholar
Right arrow Articles by Shimomura, Y.
Right arrow Articles by Bhan, A. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Shimomura, Y.
Right arrow Articles by Bhan, A. K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 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: 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.


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




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.