Hepatitis B e Antigen Induces NKG2A⁺ Natural Killer Cell Dysfunction via Regulatory T Cell-Derived Interleukin 10 in Chronic Hepatitis B Virus Infection.

ABSTRACT: Although persistent hepatitis B virus (HBV) infection is associated with natural killer (NK) cell dysfunction, it remains obscure whether HBV viral antigens are responsible for NK cell dysfunction in patients with chronic hepatitis B (CHB) infection. In this study, we found that the percentage of NK cells expressing the inhibitory receptor, NKG2A, was increased in CHB patients, and NKG2A blockade restored NK cell function. Furthermore, in CHB patients, the frequency of NK cells expressing NKG2A positively correlated with the number of regulatory T cells (Tregs) and production of interleukin-10 (IL-10) in these Tregs. Moreover, exposure of peripheral blood mononuclear cells (PBMCs) isolated from healthy controls to sera from CHB patients resulted in increased proportion of NKG2A⁺

SUBMITTER: Ma Q 

PROVIDER: S-EPMC7283553 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature