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Differential Molecular and Anatomical Basis for B Cell Migration into the Peritoneal Cavity and Omental Milky Spots¹

Simon Berberich^*, Sabrina Dähne^*, Angela Schippers, Thorsten Peters, Werner Müller, Elisabeth Kremmer, Reinhold Förster^* and Oliver Pabst^2,*

^* Institute of Immunology, Hannover Medical School, Hannover, Germany; Department of Experimental Immunology, Helmholtz Centre for Infection Research, Braunschweig, Germany; Department of Dermatology and Allergology, University of Ulm, Ulm, Germany; and Institute of Molecular Immunology, GSF National Research Center for Environment and Health, Munich, Germany

The constitutive migration of B cells from the circulation into the peritoneal cavity and back is essential for peritoneal B cell homeostasis and function. However, the molecular machinery and the anatomical basis for these migratory processes have hardly been investigated. In this study, we analyze the role of integrins as well as the role of the omentum for B2 cell migration into and out of the peritoneal cavity of mice. We demonstrate that ₄β₇ integrin-mucosal addressin cell adhesion molecule 1 interaction enables B2 cell migration from the circulation into omental milky spots but not into the peritoneum. In contrast, ₄β₁ integrin mediates direct entry of B2 cells into the peritoneal cavity as well as their retention at that site, limiting B2 cell egress via the draining parathymic lymph nodes. Surgical removal of the omentum results in a 40% reduced immigration of B2 cells from the circulation into the peritoneum but does not impair B cell exit from this compartment. In conclusion, these data reveal the existence of alternative routes for B2 cell entry into the peritoneal cavity and identify integrins as key factors for peritoneal B2 cell homeostasis, mediating B2 cell migration into and out of the peritoneal cavity as well as their retention at this site.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Deutsche Forschungsgemeinschaft Grant SFB621-A1 (to R.F.) and Forschergruppe FOR 471/2 (to W.M.). S.D. was supported by the International Research Training Group 1273, funded by the Deutsche Forschungsgemeinschaft.

² Address correspondence and reprint requests to Dr. Oliver Pabst, Institute of Immunology, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany. E-mail address: Pabst.Oliver{at}MH-Hannover.de

³ Abbreviations used in this paper: EGFP, enhanced GFP; MAdCAM-1, mucosal addressin cell adhesion molecule 1; MLN, mesenteric lymph node; PerC, peritoneal cavity; SPL, spleen.