Background: Renal fibrosis is a pathological condition which is associated with chronic inflammation. Chronic antibody-mediated rejection (CABMR) play  an increasingly critical role in kidney allograft loss and consider among one of the most important barriers that  is responsible for late term graft loss, which is results from a repetitive pattern of chronic thrombotic events and inflammatory changes, leading to cellular injury and repair. In chronic inflammation IL-6 enhance the production of  acute phase proteins  and Induction of acute phase reactions, T cell Subset differentiation, Maturation of Plasma cells, Generation of cellular and humoral immune responses against infection and Control the transition from acute to chronic inflammation by the recruitment of MCP1(monocyte chemo attractant protein 1 ). We sought to see whether IL-17A and IL-6 mediated synergistic activation of inflammation amplifier is operational in CABMR.
Methodology: CABMR patients were recruited according to revised Banff 2017 classification for the fibroblast culture from Renal Biopsy patients in vitro. Primary Fibroblast culture from CABMR patients were cultured to purity and to mimic this condition fibroblast were pre stimulated with IL-6 (20ng/ µl), IL-17(50ng/ µl), IL-6 plus IL-17 for 24 hours and culture supernatant were collected for IL-6 ELISA to see synergistic activation. Serum IL-6 levels of CABMR and Non-CABMR patients were measured by ELISA. m-RNA expression of pro-fibrotic genes; collagen 1 alpha 1 (COL1A1),Fibronectin, alpha smooth muscle actin-1(ASMA1), connective tissue growth factor (CTGF), and anti-fibrotic gene; Matrix metalloproteinase 2/Tissue inhibitor of metalloproteinase (MMP2/TIMP) was analysed with real time PCR. Student’s t-Test was used for statistical analysis in SPSS 13 software.
Results: IL-6 in sera of CABMR patients were significantly higher (p<0.001) than Non chronic rejection patients.

In comparison to IL-6 and IL-17 alone these cytokines synergistically induced more IL-6 production from renal fibroblasts.

Also, we found that concentrations of effectors of inflammation amplifiers like IL-6, CCL-20 & CCL2 (MCP-1) were significantly higher in CABMR patients compared to Non chronic rejection patients. Together IL+IL-17 signicantly increased the expression of COL1A1, ASMA1, Fibronectin,mmp2 and CCL2 against GAPDH as a housekeeping gene at mRNA compared to untreated fibroblasts.
Conclusion: Data of patients support that CBMR is perpetuated by inflammation amplifier or synergistic induction of IL-6 and IL-17.