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J Immunol. 2011 Jan 15;186(2):1268-78. doi: 10.4049/jimmunol.1002677. Epub 2010 Dec 17.

IL-2-controlled expression of multiple T cell trafficking genes and Th2 cytokines in the regulatory T cell-deficient scurfy mice: implication to multiorgan inflammation and control of skin and lung inflammation.

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1
Department of Medicine, Center for Immunity, Inflammation and Regenerative Medicine, University of Virginia, Charlottesville, VA 22908, USA. rs3wn@virginia.edu

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  • J Immunol. 2011 Apr 15;186(8):5012-3.

Abstract

Scurfy (Sf) mice bear a mutation in the Foxp3 transcription factor, lack regulatory T cells (Treg), develop multiorgan inflammation, and die prematurely. The major target organs affected are skin, lungs, and liver. “Sf mice lacking the Il2 gene (Sf.Il2–/–), despite being devoid of Treg, did not develop skin and lung inflammation, but the inflammation in liver remained [corrected]. Genome-wide microarray analysis revealed hundreds of genes that were differentially regulated among Sf, Sf.Il2(-/-), and B6 CD4(+) T cells, but the most significant changes were those encoding receptors for trafficking/chemotaxis/retention and cytokines. Our study suggests that IL-2 controls the skin and lung inflammation in Sf mice in an apparent "organ-specific" manner through two novel mechanisms: by regulating the expression of genes encoding a variety of receptors for T cell trafficking/chemotaxis/retention and by regulating Th2 cell expansion and cytokine production. Thus, IL-2 is potentially a master regulator for multiorgan inflammation and an underlying etiological factor for various diseases associated with skin and lung inflammation.

PMID:
21169543
PMCID:
PMC3136806
DOI:
10.4049/jimmunol.1002677
[Indexed for MEDLINE]
Free PMC Article

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