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The characteristic expression of B7‐H3 and B7‐H4 in liver biopsies from patients with HBV‐related acute‐on‐chronic liver failure

Hepatitis B virus (HBV) is a major public health problem, and HBV‐related acute‐on‐chronic liver failure (HBV‐ACLF) has an extremely poor prognosis due to a lack of effective treatments. B7‐H3 and B7‐H4 are two novel members of the B7 superfamily that are actively involved in regulating the pathogenesis of infectious diseases. However, the intrahepatic expression of both members in HBV‐ACLF patients has yet to be described. In this study, we analyzed the expression of B7‐H3 and B7‐H4 in HBV‐ACLF biopsies by immunohistochemistry. Our results showed that both members were observed in all HBV‐ACLF samples, and their expression was chiefly observed on infiltrating inflammatory cells and the damaged bile ducts. Immunofluorescence double staining showed that B7‐H4 was expressed chiefly on CD3+ T cells, CD68+ macrophages, CK‐18+ bile ducts, and CD31+ endothelial cells, while B7‐H3 was found on all cell types detected. The expression of the programmed death (PD)‐1 ligands, PD‐L1 and PD‐L2, was also detected in these liver tissues and they were found to be co‐expressed with B7‐H3 and B7‐H4. These results suggest that the B7‐family signaling is most likely to affect the pathogenesis of this disease, and a clear understanding of their functional roles may further elucidate the disease process.