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TitleCXCR4 promotes B cell egress from Peyer's patches
AuthorTimothy H. Schmidt, Oliver Bannard, Elizabeth E. Gray, and Jason G. Cyster
Affiliation(s)Howard Hughes Medical Institute and Department of Microbiology & Immunology, University of California, San Francisco, San Francisco, CA 94143
PublishedJEM vol. 210 no. 6 1099-1107 2013 doi: 10.1084/ jem.20122574
KeywordSilver LED 415
Snippet... 4 A, middle). A Silver LED 415 (Prizmatix), set to maximum intensity, with a high numerical aperture polymer optical fiber (core diameter, 1.5 mm) light guide and fiber collimator, was used as a 415 nm violet light source. Each PP was exposed for 3 min (Fig. ...
AbstractPeyer’s patches (PPs) play a central role in supporting B cell responses against intestinal antigens, yet the factors controlling B cell passage through these mucosal lymphoid tissues are incompletely understood. We report that, in mixed chimeras, CXCR4-deficient B cells accumulate in PPs compared with their representation in other lymphoid tissues. CXCR4-deficient B cells egress from PPs more slowly than wild-type cells, whereas CXCR5-deficient cells egress more rapidly. The CXCR4 ligand, CXCL12, is expressed by cells adjacent to lymphatic endothelial cells in a zone that abuts but minimally overlaps with the CXCL13+ follicle. CXCR4-deficient B cells show reduced localization to these CXCL12+ perilymphatic zones, whereas CXCR5-deficient B cells preferentially localize in these regions. By photoconverting KikGR-expressing cells within surgically exposed PPs, we provide evidence that naive B cells transit PPs with an approximate residency half-life of 10 h. When CXCR4 is lacking, KikGR+ B cells show a delay in PP egress. In summary, we identify a CXCL12hi perilymphatic zone in PPs that plays a role in overcoming CXCL13-mediated retention to promote B cell egress from these gut-associated lymphoid tissues.


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