@article {4608,
	title = {Cutting edge: the role of IFN-α receptor and MyD88 signaling in induction of IL-15 expression in vivo.},
	journal = {Journal of Immunology},
	volume = {188},
	year = {2012},
	month = {2012 Mar 15},
	pages = {2483-7},
	abstract = {<p>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.</p>
},
	issn = {1550-6606},
	doi = {10.4049/jimmunol.1103609},
	author = {Colpitts, Sara L and Stoklasek, Thomas A and Plumlee, Courtney R and Obar, Joshua J and Guo, Caiying and Lefran\c cois, Leo}
}
