Notably, parallel analysis in aorta samples revealed upregulation of endothelial dysfunction (Icam1, Vcam1) and vascular inflammation markers (Ccl2, Olr1), together with a trend towards increased expression of the CXCR3 ligand, Cxcl10. Importantly CXCR3+LFA-1+ CD4+ and CD8+ T cell effectors were markedly enhanced at systemic level, thus providing insights into the mechanistic link between highly differentiated T cells, endothelial dysfunction and vascular inflammation. The gene discussed is CXCR3; the disease is inflammation.