Document Type

Article

Disciplines

Life Sciences | Medicine and Health Sciences

Abstract

Interleukin-15 (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 IFNAR expression for EmGFP/IL-15 upregulation after VSV 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.

Comments

J Immunol. Author manuscript; available in PMC 2013 March 15. Published in final edited form as: J Immunol. 2012 March 15; 188(6): 2483–2487. Published online 2012 February 10. doi: 10.4049/jimmunol.1103609 PMCID: PMC3294000 NIHMSID: NIHMS351774

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