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pubmed-article:19003934pubmed:abstractTextOrgan-specific homing of lymphoid cells depends on the expression of tissue-specific adhesion molecules and production of specific chemokines. CCL25 (TECK) and CCL28 (MEC) have been reported to direct circulating memory/effector B cells to mucosal tissues. Here, we examined if differential responsiveness to mucosal and systemic chemokines could explain the differential migration pattern of circulating human antibody-secreting cells (ASC), induced by mucosal and systemic immunization. There was a robust migration of specific IgA- and IgM-ASC induced by Salmonella vaccination toward the mucosal chemokines CCL25 and CCL28. In contrast, tetanus-specific ASC migrated to the systemic chemokine CXCL12 (SDF-1alpha) and showed no response to CCL25 or CCL28, not even tetanus-specific IgA-ASC. Cell sorting experiments demonstrated that Salmonella-specific ASC co-expressed CCR9 and CCR10. Our results show that induction site, rather than isotype commitment, determines the chemokine responsiveness and migration pattern of human effector B cells.lld:pubmed
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pubmed-article:19003934pubmed:pagination3327-38lld:pubmed
pubmed-article:19003934pubmed:dateRevised2010-2-24lld:pubmed
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pubmed-article:19003934pubmed:year2008lld:pubmed
pubmed-article:19003934pubmed:articleTitleHuman IgA-secreting cells induced by intestinal, but not systemic, immunization respond to CCL25 (TECK) and CCL28 (MEC).lld:pubmed
pubmed-article:19003934pubmed:affiliationDepartment of Microbiology and Immunology, Göteborg University Vaccine Research Institute, The Sahlgrenska Academy, The University of Gothenburg, Gothenburg, Sweden.lld:pubmed
pubmed-article:19003934pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:19003934pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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