Defects in endomembrane dynamics associated with Rab27a deficiency cause defective endosomal-toll-like receptor sensing and cytokine secretion in neutrophils and plasmacytoid dendritic cells.

We collected gene expression data (RNAseq) from mature Ly6G+ neutrophils isolated from mice bone marrow. The samples were obtained from both Wild-Type and RAB27A knockout mice. These neutrophils were either treated with CpG, a TLR9 agonist, for 6 hours or left untreated. The transcriptional data complement the study of the role of Rab27a-mediated vesicular trafficking on signaling pathways downstream of TLR9 activation and cytokine secretion in immune cells.