Regulatory B cells suppress imiquimod-induced, psoriasis-like skin inflammation

Koichi Yanaba, Masahiro Kamata, Nobuko Ishiura, Sayaka Shibata, Yoshihide Asano, Yayoi Tada, Makoto Sugaya, Takafumi Kadono, Thomas F. Tedder, Shinichi Sato

研究成果: Article査読

77 被引用数 (Scopus)


Psoriasis is an inflammatory cutaneous disorder characterized by marked epidermal thickening and Th1 and Th17 cell infiltration. At present, the contribution of B cells to the pathogenesis of psoriasis is unclear. In mice, topical application of imiquimod induces inflamed skin lesions and serves as an experimental animal model for human psoriasis. In this study, we showed that imiquimod-induced skin inflammation was more severe in CD19-/- than WT mice. These inflammatory responses were negatively regulated by a unique IL-10-producing CD1dhiCD5+ regulatory B cell subset (B10 cells) that was absent in CD19-/- mice and represented only 1-2% of splenic B220+ cells in WT mice. Splenic B10 cells entered the circulation and migrated to draining LNs during imiquimod-induced skin inflammation, thereby suppressing IFN-γ and IL-17 production. Furthermore, adoptive transfer of these B10 cells from WT mice reduced inflammation in CD19-/- mice. The present findings provide direct evidence that B10 cells regulate imiquimod-induced skin inflammation and offer insights into regulatory B cell-based therapies for the treatment of psoriasis.

ジャーナルJournal of Leukocyte Biology
出版ステータスPublished - 2013 10月

ASJC Scopus subject areas

  • 免疫アレルギー学
  • 免疫学
  • 細胞生物学


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