In a model of intestinal Yersinia pseudotuberculosis infection, inflammatory macrophages derived from bone-marrow monocytes (CCR2-dependent migration) accumulate and positively regulate the differentiation of CD103− TRM at the site of inflammation via provision of signal 3 cytokines (IL-12 and type I IFNs) that dampen CD103 expression (40, 47). This evidence concerns the gene ITGAE and Yersinia pseudotuberculosis infectious disease.