In conclusion, HK-2 cells stimulated with TGF-b 1 induced activation of LFA-1 on PBMCs by increased CXCL12. The direct interaction of LFA-1 on PBMCs and ICAM-1 on HK-2 cells activated ERK1/2 signaling to accelerate the part of EMT of HK-2 cells induced by TGF-b 1. These results suggested that drugs that can block the interaction of LFA-1 and ICAM-1 could be an option to treat renal fibrosis.