Preoperative CD52 Level Predicts Graft Survival following Kidney Transplantation

Abstract

Several factors have been reported to affect graft survival following kidney transplantation. CD52 molecules may increase T cell proliferation and activation, which may contribute to acute graft rejection and graft survival. In the current study, we studied the possible value of preoperative CD52 levels in predicting graft survival following renal transplantation. Ninety-six patients with end-stage renal disease who had kidney transplantation were included in the study from our prospective cohort. Blood samples were taken one day before surgery, and plasma CD52 levels were measured using ELISA (Cloud-Clone Corp., Houston, TX, USA). Acute rejection, acute tubular necrosis, delayed graft function, graft loss, BK infection, cytomegalovirus infection, and graft survival were evaluated. The mean age of recipients was 50:08 ± 12:82 years, and 64.6% were male. The incidence of delayed graft function, acute rejection, graft loss (p < 0:01), BK virus infection, and serum creatinine levels were significantly higher in recipients with high preoperative CD52 levels six months after transplantation (p < 0:05). Kaplan-Meier analysis revealed that three-year graft survival was significantly higher in patients with low preoperative CD52 levels (p < 0:0001). Univariate and multivariate Cox regression analyses showed that serum creatinine levels (hazard ratio ½HR = 1:7, p < 0:05), acute rejection (HR = 2:919, p < 0:05), and preoperative CD52 levels (HR = 3:114, p < 0:05) were independent prognostic factors for graft survival after kidney transplantation. We showed that high preoperative CD52 levels are associated with higher rates of acute rejection, delayed graft function, and BK virus infection and lower rates of graft survival after kidney transplantation.

Flotillin-2 dampens T cell antigen-sensitivity and functionality

“…Specifically, even in the naive state, Flot2 CD4 CD4 + T cells demonstrated higher expression levels of spliced Ppia, Cd52, and Malat1 (Figure 6j). These genes are known to positively regulate T cell proliferation, activation, as well as to enhance cytotoxic T cell differentiation and cytokine production (45)(46)(47)(48)(49)(50). This suggests that while gene expression alterations remain consistent, differences in isoform usage may contribute to variations in T cell activation between Flot2 WT and Flot2 CD4 CD4 + T cells.…”