ArticleVirus research2026
CD72 downregulation is associated with increased CD5+ B cell proliferation and IL-10 production via ERK/Syk signaling in chronic HBV infection-associated liver disease.
Article in Virus research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundChronic hepatitis B virus (HBV) infection is characterized by selective impairment of virus-specific immune responses. However, progressive liver disease, particularly cirrhosis, is associated with broader immune remodeling that may influence B cell phenotype and function. CD72 is a negative regulator of B cell receptor (BCR) signaling but its role in CD5+B cell regulation under these conditions remains unclear.
methodsPeripheral Blood Mononuclear cells (PBMCs) were isolated from 51 HBV-infected patients at differing disease stages and 24 healthy controls by density gradient centrifugation. B cells were isolated using CD19 microbeads. CD72 expression, B cell proliferation, protein phosphorylation and cytokine secretion were assessed by flow cytometry, BrdU assay, Western blotting, lentiviral shRNA-mediated knockdown, RT-qPCR and ELISA.
resultsCD72 expression significantly decreased in HBV patient CD5+ B cells but increased in CD5- B cells, correlating negatively with CD5 expression. CD72 knockdown enhanced CD5+ B cell proliferation 2.1-fold (P < 0.01) and increased IL-10, IL-6 and IgM secretion. This phenotype depended on ERK/Syk activation, evidenced by elevated p-ERK levels and abolished proliferation upon ERK/Syk inhibition (P < 0.001). No effects were observed in CD5- B cells.
conclusionCD72 downregulation enhanced the activation and regulatory function of CD5+B cells through ERK/Syk signaling under conditions associated with chronic liver disease. These findings suggest that alterations in CD72 expression may contribute to B cell functional remodeling in the context of HBV-related liver pathology.
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