The Expression Of Costimulatory Molecule Cd28, Icos, Pd-1 And Ctla-4 In Peripheral Blood Of Sle Patients

Objective: To demonstrate whether the costimulatory molecules CD28, ICOS, PD-1 and CTLA-4 were participated in pathogenesis of systemic lupus erythematosus(SLE), we detected the expression of those costimulatory molecules by immunofluorescence and flow cytometry(FCM), in the meantime we analyzed the correlation between the expression of those costimulatory molecules and SLE diseases activity index(SLEDAI).Method: We collected the peripheral blood of 23 SLE patients(only 8 of them were non-active as self-control group) and 30 health people were volunteered. We detected the expression levers of those costimulatory molecules on the surface of CD4+T lymphocytes in peripheral blood of active, non-active SLE and healthy people by immunofluorescence and flow cytometry.Result: In patients with SLE, there were no significant difference between the expression levers of CD28 and ICOS which were compared with the health group(P>0.05), the expression of PD-1 was significantly higher than health group(P<0.0001), and the expression of CTLA-4 was significantly different from the healthy group(P<0.01). In 23 active patients and 8 non-active patients, there was no statistically significant difference between the expression levers of three costimulatory molecules(P>0.05) except PD-1. In the active group, the expression of PD-1 was significantly higher(P<0.05) than non-active group. In the self-control group, the expression levers of CD28 and PD-1 were higher than non-active group(P<0.05,P=0.01), but there were no difference between the expression levers of ICOS and CTLA-4(P>0.05). Moreover, there was no relation between the expression levers of those four costimulatory molecules and SLEDAI.Conclusion: In conclusion, we proposed that both PD-1 and CTLA-4 may be involved in the pathogenesis of SLE, but it needs further study to find out how they activated the disease. The data showed that there was difference between the expression of CD28 with its self-control group, so it probably was participated in pathogenesis of disease, but ICOS may be less to do with the pathogenesis of SLE.