期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 111, 期 7, 页码 1001-1010出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI200317244
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资金
- NHLBI NIH HHS [P50 HL067674, P01 HL067674, HL-67674] Funding Source: Medline
- NIAID NIH HHS [AI-47822, T32 AI007290, R21 AI047822, R37 AI047822, R01 AI047822] Funding Source: Medline
- NIDDK NIH HHS [DK-56339, P30 DK056339] Funding Source: Medline
- NIGMS NIH HHS [GM-37734, R01 GM037734, R37 GM037734] Funding Source: Medline
The dissemination of IgA-dependent immunity between mucosal sites has important implications for mucosal immunoprotection and vaccine development. Epithelial cells in diverse gastrointestinal and nonintestinal mucosal tissues express the chemokine MEC/CCL28. Here we demonstrate that CCR10, a receptor for MEC, is selectively expressed by IgA Ab-secreting cells (large s/cIgA(+)CD38(hi)CD19(int/-)CD20(-)), including circulating IgA(+) plasmablasts and almost all IgA(+) plasma cells in the salivary gland, small intestine, large intestine, appendix, and tonsils. Few T cells in any mucosal tissue examined express CCR10. Moreover, tonsil IgA plasmablasts migrate to MEC, consistent with the selectivity of CCR10 expression. In contrast, CCR9, whose ligand TECK/CCL25 is predominantly restricted to the small intestine and thymus, is expressed by a fraction of IgA Ab-secreting cells and almost all T cells in the small intestine, but by only a small percentage of plasma cells and plasmablasts in other sites. These results point to a unifying role for CCR10 and its mucosal epithelial ligand MEC in the migration of circulating IgA plasmablasts and, together with other tissue-specific homing mechanisms, provides a mechanistic basis for the specific dissemination of IgA Ab-secreting cells after local immunization.
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