Journal
JOURNAL OF IMMUNOLOGY
Volume 186, Issue 2, Pages 1268-1278Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1002677
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Funding
- National Institutes of Health [DE-01759, AR-051203, AR-047988, AR-049449, HL084422]
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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, pancreas, submandibular gland, and colon remained. 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. The Journal of Immunology, 2011, 186: 1268-1278.
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