deficiency in myeloid cells increases susceptibility toinfection in mice.

Abstract

v-Maf avian musculoaponeurotic fibrosarcoma oncogene homolog B () is a candidate gene associated with early tuberculosis onset identified by a genome-wide association study. Here, we investigated the role ofin susceptibility to() infection in myeloid-specific-knockout (-cKO) miceinfection was performed bothusing bone marrow-derived macrophages (BMMs) from-cKO mice andin-cKO mice. The absence ofpromotedproliferation in BMMs. RNA sequencing (RNA-seq) revealed activation of the metabolic process and impairment of the response to type I interferons (IFNs) in-infected BMMs from-cKO mice, which conforms to our previous findings in-infected human macrophages withknockdown.deficiency increased mortality and bacterial burden in the lungs and spleens duringinfection in mice. RNA-seq revealed weakened leukocyte or lymphocyte chemotaxis in-infected-cKO mouse lungs. Flow cytometry demonstrated an alteration in the proportion of immune cells in-infected mouse lungs due todeficiency. Together,in myeloid cells is involved not only in the functional antibacterial process of macrophages but also in immune cell recruitment in the lungs, thereby contributing to host defense againstinfection.