CCL2 and primary biliary cholangitis: Further in vitro study revealed that oxidative stress- and DNA damage-induced senescent BECs exhibited stronger secretion of chemokines (CCL-2/3/4/5, CX3CL-1, CXCL-1, CXCL-2, CXCL-10, and CXCL-16), thereby attracting monocyte/macrophage-like RAW264.7 cells, which suggested that the influence of senescent cholangiocytes on the pathogenesis of PBC was likely achieved by their environmental modulation (116).