Poster 21. Broadly profiling the activation status of circulating immune cells in c-aABMR reveals increased CD38 and CD16 expression on monocytes and NK cells




Thursday 14 march 2019

12:45 - 12:48h

Categories: Klinisch, Postersessie

Parallel session: Postersessies 5 - Clinical


K.A. Sablik, N.H.R. Litjens, M. Klepper, M.G.H. Betjes

Dept. of Internal Medicine, Division of Nephrology and Kidney Transplantation, Erasmus University Medical Center, Rotterdam, The Netherlands.


Background: Chronic-active antibody mediated rejection (c-aABMR) contributes significantly to late renal allograft failure. Non-invasive biomarkers of c-aABMR are currently not available but could be valuable for early detection. In this study the activation profiles of relevant immune cell populations in peripheral blood of patients with c-aABMR were evaluated as potential biomarker.

Methods: The peripheral blood mononuclear cells of the kidney transplant recipients included were used for flow cytometric analysis. A panel of monoclonal antibodies was used designed to characterize both the specific cell type (T and B cells, γδT cells, NK cells and monocytes ) and their activation status. Cases with biopsy proven c-aABMR (c-aABMRpos, N=25) were compared to matched controls (c-aABMRneg, N=25).

Results: No significant differences were found in the total percentage and distribution of NK cells, B cells and T cells. There was however a higher percentage of monocytes present in c-aABMRpos cases (19.5% vs. 14.4%, p<0.05). Additionally, differences were found in activation status of circulating monocytes, NK cells and γδT cells. The c-aABMRpos cases had a significantly higher percentage of monocytes expressing the activation marker CD38 (p=0.04) as well as higher expression of CD38 on NK cells (p=0.02). CD16 (FcγIII receptor) expression on NK cells was significantly higher in c-aABMRpos cases (MFI 56965 vs. 34345, p<0.01) but significantly lower in γδT cells (MFI 837 vs. 1277, p=0.02). Although statistically significant, these differences were not sufficient to readily identify patients with c-aABMR.

Conclusions: Cases with c-aABMR express a different CD16 and CD38 expression profile on circulating NK cells, γδT cells and monocytes. Increased CD16 expression on circulating NK cells suggest that an interaction with antibodies on renal endothelial cells has taken place.