Recipients with recurrent HCV-induced allograft inflammation and fibrosis/cirrhosis presented a significant increase in the frequency of HCV-specific CD4+ Th17 cells; as well as proinflammatory mediators (IL-17, IL-1β, IL-6, IL-8, and MCP-1). Recurrent patients despite demonstrating increased Treg frequency, this did not inhibit HCV-specific CD4+ Th17 cells. Here, CCL2 is linked to fibrosis.