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Abstract: PO2390

IL-6- and IL-17-Mediated Inflammation Amplifier Loop in Chronic Antibody-Mediated Rejection

Session Information

Category: Transplantation

  • 1901 Transplantation: Basic


  • Prasad, Narayan, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
  • Singh, Mantabya K., Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
  • Agarwal, Vikas, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Renal fibrosis is a pathological condition associated with chronic inflammation that may result from a cellular injury and repair and result into late graft loss. In chronic inflammation, IL-6 combined with sIL-6R with gp130, together these complex activate the IL-6 trans signalling and control the transition from acute to chronic inflammation by the recruitment of MCP1 by activating NFkB and STAT3 signaling. We studied whether IL-17A and IL-6 mediated synergistic activation of inflammation amplifier loop is operational in CABMR.


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 hrs 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. mRNA expression of pro-fibrotic genes; COL1A1, FN1, ASMA1, and anti-fibrotic gene; MMP2/TIMP was analyzed with real-time PCR. Student’s t-test was used for statistical analysis in SPSS 17 software.


IL-6 in sera of CABMR patients was significantly higher (p<0.001) than non-rejection patients. In comparison to IL-6 and IL-17 alone these cytokines synergistically induced more IL-6 production from renal fibroblasts(Fig 1). Together IL+IL-17 signicantly increased the expression of COL1A1, ASMA1, Fibronectin and CCL2(MCP1) and reduced expression of MMP2 gene against GAPDH gene compared to alone IL-6, IL-17 and untreated fibroblasts.


CBMR is perpetuated by inflammation amplifier or synergistic induction of IL-6 and IL-17 which results in chronic inflammation and Allograft rejection. Anti-Il-6 may attenuate the CABMR related injury.

Amplifier Loop in culture supernatent. Serum IL-6 con. in CABMR.


  • Government Support - Non-U.S.