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

Published

Journal Article

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 CD1d(hi)CD5(+) 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.

Full Text

Duke Authors

Cited Authors

  • Yanaba, K; Kamata, M; Ishiura, N; Shibata, S; Asano, Y; Tada, Y; Sugaya, M; Kadono, T; Tedder, TF; Sato, S

Published Date

  • October 2013

Published In

Volume / Issue

  • 94 / 4

Start / End Page

  • 563 - 573

PubMed ID

  • 23630391

Pubmed Central ID

  • 23630391

Electronic International Standard Serial Number (EISSN)

  • 1938-3673

Digital Object Identifier (DOI)

  • 10.1189/jlb.1112562

Language

  • eng

Conference Location

  • United States