CD19 expression in B cells regulates atopic dermatitis in a mouse model.

Published

Journal Article

Atopic dermatitis is an inflammatory cutaneous disorder characterized by dry skin and relapsing eczematous skin lesions. Besides antibody production, the contribution of B cells to the pathogenesis of atopic dermatitis is unclear. In mice, repeated epicutaneous sensitization with ovalbumin induces inflamed skin lesions resembling human atopic dermatitis and therefore serves as an experimental model for this condition. To investigate the role of B cells in a murine model of atopic dermatitis, ovalbumin-sensitized allergic skin inflammation was assessed in mice lacking CD19. In ovalbumin-sensitized skin from CD19-deficient mice, the number of eosinophils and CD4(+) T cells was reduced, and both epidermal and dermal thickening were decreased. Following in vitro stimulation with ovalbumin, CD19 deficiency significantly reduced the proliferation of CD4(+), but not CD8(+), T cells from spleen and draining lymph nodes. Furthermore, splenocytes and draining lymph node cells from ovalbumin-sensitized CD19-deficient mice secreted significantly less IL-4, IL-13, and IL-17 than ovalbumin-sensitized wild-type mice. These results suggest that CD19 expression in B cells plays a critical role in antigen-specific CD4(+) T-cell proliferation and T helper 2 and 17 responses in a murine model of atopic dermatitis. Furthermore, the present findings may have implications for B-cell-targeted therapies for the treatment of atopic dermatitis.

Full Text

Duke Authors

Cited Authors

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

Published Date

  • June 2013

Published In

Volume / Issue

  • 182 / 6

Start / End Page

  • 2214 - 2222

PubMed ID

  • 23583649

Pubmed Central ID

  • 23583649

Electronic International Standard Serial Number (EISSN)

  • 1525-2191

Digital Object Identifier (DOI)

  • 10.1016/j.ajpath.2013.02.042

Language

  • eng

Conference Location

  • United States