CC Chemokine Ligands 25 and 28 Play Essential Roles in Intestinal Extravasation of IgA Antibody-Secreting Cells

DOI PDF PubMed 被引用文献15件 オープンアクセス
  • Kunio Hieshima
    Department of Microbiology, Kinki University School of Medicine , Osaka ,
  • Yuri Kawasaki
    Department of Microbiology, Kinki University School of Medicine , Osaka ,
  • Hitoshi Hanamoto
    Department of Internal Medicine, Division of Haematology, Nephrology, and Rheumatology, Kinki University School of Medicine , Osaka ,
  • Takashi Nakayama
    Department of Microbiology, Kinki University School of Medicine , Osaka ,
  • Daisuke Nagakubo
    Department of Microbiology, Kinki University School of Medicine , Osaka ,
  • Akihisa Kanamaru
    Department of Internal Medicine, Division of Haematology, Nephrology, and Rheumatology, Kinki University School of Medicine , Osaka ,
  • Osamu Yoshie
    Department of Microbiology, Kinki University School of Medicine , Osaka ,

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公開日
2004-09
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.173.6.3668
公開者
Oxford University Press (OUP)

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<jats:title>Abstract</jats:title> <jats:p>CCL25 (also known as thymus-expressed chemokine) and CCL28 (also known as mucosae-associated epithelial chemokine) play important roles in mucosal immunity by recruiting IgA Ab-secreting cells (ASCs) into mucosal lamina propria. However, their exact roles in vivo still remain to be defined. In this study, we first demonstrated in mice that IgA ASCs in small intestine expressed CCR9, CCR10, and CXCR4 on the cell surface and migrated to their respective ligands CCL25, CCL28, and CXCL12 (also known as stromal cell-derived factor 1), whereas IgA ASCs in colon mainly expressed CCR10 and CXCR4 and migrated to CCL28 and CXCL12. Reciprocally, the epithelial cells of small intestine were immunologically positive for CCL25 and CCL28, whereas those of colon were positive for CCL28 and CXCL12. Furthermore, the venular endothelial cells in small intestine were positive for CCL25 and CCL28, whereas those in colon were positive for CCL28, suggesting their direct roles in extravasation of IgA ASCs. Consistently, in mice orally immunized with cholera toxin (CT), anti-CCL25 suppressed homing of CT-specific IgA ASCs into small intestine, whereas anti-CCL28 suppressed homing of CT-specific IgA ASCs into both small intestine and colon. Reciprocally, CT-specific ASCs and IgA titers in the blood were increased in mice treated with anti-CCL25 or anti-CCL28. Anti-CXCL12 had no such effects. Finally, both CCL25 and CCL28 were capable of enhancing α4 integrin-dependent adhesion of IgA ASCs to mucosal addressin cell adhesion molecule-1 and VCAM-1. Collectively, CCL25 and CCL28 play essential roles in intestinal homing of IgA ASCs primarily by mediating their extravasation into intestinal lamina propria.</jats:p>

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