The Journal of Experimental Medicine
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Published online 23 October 2006 doi:10.1084/jem.20061041
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 11, 2541-2550
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ARTICLE

 Regulation of B1 cell migration by signals through Toll-like receptors

Seon-ah Ha1, Masayuki Tsuji1, Keiichiro Suzuki1, Bob Meek1, Nobutaka Yasuda2, Tsuneyasu Kaisho3, and Sidonia Fagarasan1

1 Laboratory for Mucosal Immunity and 2 Department of Veterinary Medicine, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Tokyo 113-8657, Japan
3 Laboratory for Host Defense, RIKEN, Research Center for Allergy and Immunology, Yokohama, Kanagawa 230-0045, Japan

CORRESPONDENCE Sidonia Fagarasan: sidonia-f{at}rcai.riken.jp

Peritoneal B1 cells are known to generate large amounts of antibodies outside their residential site. These antibodies play an important role in the early defense against bacteria and viruses, before the establishment of adaptive immune responses. Although many stimuli, including antigen, lipopolysaccharide, or cytokines, have been shown to activate B1 cells and induce their differentiation into plasma cells, the molecular signals required for their egress from the peritoneal cavity are not understood. We demonstrate here that direct signals through Toll-like receptors (TLRs) induce specific, rapid, and transient down-regulation of integrins and CD9 on B1 cells, which is required for detachment from local matrix and a high velocity movement of cells in response to chemokines. Thus, we revealed an unexpected role for TLRs in governing the interplay between integrins, tetraspanins, and chemokine receptors required for B1 cell egress and, as such, in facilitating appropriate transition from innate to adaptive immune responses.

Abbreviations used: M{Phi}, macrophages; MyD88, myeloid differentiation primary response gene 88; MZ, marginal zone; PTX, pertussis toxin; S1P1, sphingosine-1-phosphate receptor 1; Tg, transgenic; TLR, Toll-like receptor.


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