The present study is the first to demonstrate the role of siglec-E during HFD-induced AT inflammation by redistributing and increasing the number of M1 macrophage, CXCR3-expressing CD8+T cell, neutrophils, NK, and NKT cells while concomitantly reducing DCs in AT in genetically deficient siglec E mice. This evidence concerns the gene CXCR3 and ataxia telangiectasia.