Balanced responsiveness to chemoattractants from adjacent zones determines B-cell position

Karin Reif, Eric H. Ekland, Lars Ohl, Hideki Nakano, Martin Lipp, Reinhold Förster and Jason G. Cyster ()
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Karin Reif: University of California San Francisco
Eric H. Ekland: University of California San Francisco
Lars Ohl: University Clinic for Surgery, Nikolaus-Fiebiger-Center
Hideki Nakano: Toho University School of Medicine
Martin Lipp: Molecular Tumorgenetics and Immunogenetics, Max-Delbrück-Center for Molecular Medicine
Reinhold Förster: University Clinic for Surgery, Nikolaus-Fiebiger-Center
Jason G. Cyster: University of California San Francisco

Nature, 2002, vol. 416, issue 6876, 94-99

Abstract: Abstract B lymphocytes re-circulate between B-cell-rich compartments (follicles or B zones) in secondary lymphoid organs, surveying for antigen. After antigen binding, B cells move to the boundary of B and T zones to interact with T-helper cells1,2,3. Despite the importance of B–T-cell interactions for the induction of antibody responses, the mechanism causing B-cell movement to the T zone has not been defined. Here we show that antigen-engaged B cells have increased expression of CCR7, the receptor for the T-zone chemokines4,5 CCL19 and CCL21, and that they exhibit increased responsiveness to both chemoattractants. In mice lacking lymphoid CCL19 and CCL21 chemokines, or with B cells that lack CCR7, antigen engagement fails to cause movement to the T zone. Using retroviral-mediated gene transfer we demonstrate that increased expression of CCR7 is sufficient to direct B cells to the T zone. Reciprocally, overexpression of CXCR5, the receptor for the B-zone chemokine CXCL13, is sufficient to overcome antigen-induced B-cell movement to the T zone. These findings define the mechanism of B-cell relocalization in response to antigen, and establish that cell position in vivo can be determined by the balance of responsiveness to chemoattractants made in separate but adjacent zones.

Date: 2002
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DOI: 10.1038/416094a

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