Crosstalk between innate and adaptive immunity in hepatitis B virus infection

Abstract

Hepatitis B virus (HBV) infection is a major public health problem worldwide. HBV is not directly cytotoxic to infected hepatocytes; the clinical outcome of infection results from complicated interactions between the virus and the host immune system. In acute HBV infection, initiation of a broad, vigorous immune response is responsible for viral clearance and self-limited inflammatory liver disease. Effective and coordinated innate and adaptive immune responses are critical for viral clearance and the development of long-lasting immunity. Chronic hepatitis B patients fail to mount efficient innate and adaptive immune responses to the virus. In particular, HBV-specific cytotoxic T cells, which are crucial for HBV clearance, are hyporesponsiveness to HBV infection. Accumulating experimental evidence obtained from the development of animal and cell line models has highlighted the importance of innate immunity in the early control of HBV spread. The virus has evolved immune escape strategies, with higher HBV loads and HBV protein concentrations associated with increasing impairment of immune function. Therefore, treatment of HBV infection requires inhibition of HBV replication and protein expression to restore the suppressed host immunity. Complicated interactions exist not only between innate and adaptive responses, but also among innate immune cells and different components of adaptive responses. Improved insight into these complex interactions are important in designing new therapeutic strategies for the treatment HBV infection. In this review, we summarize the current knowledge regarding the cross-talk between the innate and adaptive immune responses and among different immunocytes in HBV infection.

Keywords: Adapative immune; Crosstalk; Hepatitis B virus; Innate immune.

Figure 1

Expressions and activation of toll-like receptors in innate and adaptive immune cells in controlling hepatitis B virus infection. HBV: Hepatitis B virus; NPCs: Non-parenchymal cells; NK: Natural killer; IFN: Interferon; TLRs: Toll-like receptors; ISG: Interferon-stimulated genes; RIG-I: Retinoic acid inducible gene I; IRF: Interferon-regulatory factors; NF-κB: Nuclear factor κB; PBMCs: Periperal blood mononuclear cells; MDA5: Melanoma differentiation associated gene 5; DCs: Dendritic cells.