Increased NKG2D expressing NK cells in patients with chronic HBV infection

Abstract

Abstract Introductions Hepatitis B virus (HBV) infection remains a significant health issue worldwide. It is a major cause of cirrhosis, HCC and liver failure. A large number of studies showed that host immune responses are the key factor for HBV clearance and persistence. In here, we investigated the role of NK cells in chronic HBV infections. Methods We compared the expression frequency, and functionality of NKGs and KIRs repertoire on NK cells in 170 samples by multi-colour flow cytometry. To further investigate the functionality of the NK cells, we performed K562 target cell killing assay and cytokine driven perforin released assay. Results The percentage of circulation and liver resident NK cells did not significantly alter in HBV patients compared to the healthy controls (HCs). Enrichment of NK cells was observed in the healthy controls but not in the HBV infected patients. The intracellular expression of Granzyme B was significantly reduced in NK cells derived from HBV-infected patients as compared to HCs. No differences were observed in the expression of NKG2A and NKG2C. Interestingly, the levels of NKG2D was significantly increased in the circulating NK cells of HBV infection but not in the liver resident NK cells. The K562 target cell killing ability and IFN-gamma production correlated with the NKG2D expression, particularly in the HBV patients as compared to HCs. Conclusions Our study demonstrated that NK cells activity and status might play an important role in controlling HBV infection.