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David T. Woodley, MD; Gene H. Kim, MD

Arch Dermatol. 2009;145(6):713-714.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

INTRODUCTION

TGF-Beta–Dependent Suppressive Function of Tregs Requires Wild-Type Levels of CD18 in a Mouse Model of Psoriasis
Wang H, Peters T, Sindrilaru A, et al
J Clin Invest. 2008;118(7):2629-2639

Dysfunctional Tregs have been identified in individuals with psoriasis. However, their role in the pathogenesis of the disease remains unclear. Here we explored the effect of diminished C18 (beta2 integrin) expression on the function of CD4+CD25+CD127(–) Tregs using the Cd18 hypomorphic PL/J mouse model of psoriasis that closely resembles the human disease. We found that reduced C18 expression impaired cell-cell contact between Tregs and DCs [dendritic cells]. This led to dysfunction of Tregs, which both failed to suppress the pathogenic T cells and promoted the onset and severity of the disease. This failure was TGF-beta-dependent, as Tregs derived from Cd18^hypo PL/J mice had diminished TGF-beta1 expression. Adoptive transfer of Tregs expressing wild-type levels of . . . [Full Text of this Article]

COMMENT

AUTHOR INFORMATION

Department of Dermatology, The Keck School of Medicine, University of Southern California, Los Angeles

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