Cutting edge: the role of IFN-α receptor and MyD88 signaling in induction of IL-15 expression in vivo.

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Journal of Immunology. 2012 Mar 15;188(6):2483-7. doi: 10.4049/jimmunol.1103609

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Colpitts SL, Stoklasek TA, Plumlee CR, Obar JJ, Guo C, cois L

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Abstract

IL-15 plays a multifaceted role in immune homeostasis, but the unreliability of IL-15 detection has stymied exploration of IL-15 regulation in vivo. To visualize IL-15 expression, we created a transgenic mouse expressing emerald-GFP (EmGFP) under IL-15 promoter control. EmGFP/IL-15 was prevalent in innate cells including dendritic cells (DCs), macrophages, and monocytes. However, DC subsets expressed varying levels of EmGFP/IL-15 with CD8(+) DCs constitutively expressing EmGFP/IL-15 and CD8(-) DCs expressing low EmGFP/IL-15 levels. Virus infection resulted in IL-15 upregulation in both subsets. By crossing the transgenic mice to mice deficient in specific elements of innate signaling, we found a cell-intrinsic dependency of DCs and Ly6C(+) monocytes on IFN-α receptor expression for EmGFP/IL-15 upregulation after vesicular stomatitis virus infection. In contrast, myeloid cells did not require the expression of MyD88 to upregulate EmGFP/IL-15 expression. These findings provide evidence of previously unappreciated regulation of IL-15 expression in myeloid lineages during homeostasis and following infection.

PMID: 22327071 [PubMed - indexed for MEDLINE]

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Cutting edge: the role of IFN-α receptor and MyD88 signaling in induction of IL-15 expression in vivo.

Abstract

PMID: 22327071 [PubMed - indexed for MEDLINE]

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