Compensatory relationships determine the impact of TGF-β on the humoral immune response to hepatitis B surface antigen - PubMed
5 hours ago
- #Hepatitis B
- #TGF-beta
- #Humoral Immunity
- Chronic hepatitis B virus (HBV) infection remains a global health issue despite an effective vaccine, with about 250 million chronic cases and one million annual deaths.
- The hepatitis B surface antigen (HBsAg)-specific antibody (HBsAb) is protective and key to a functional cure, but early regulatory factors influencing HBsAg seroconversion are not well understood.
- Using an adeno-associated virus (AAV)-HBV mouse model, C57BL/6 mice showed poor HBsAb responses, while BALB/c mice efficiently seroconverted HBsAg.
- Inhibiting TGF-β, IL-10, or regulatory T cells (Tregs) did not affect serum HBsAg levels in C57BL/6 mice, but TGF-β depletion in BALB/c mice abolished the humoral response to HBsAg.
- Neutralizing IL-10, blocking CTLA-4, or depleting Tregs alone had no impact on the HBsAb response in BALB/c mice.
- Treg depletion in the absence of TGF-β restored HBsAg clearance independently of IL-10 and CTLA-4, highlighting compensatory interactions in immune regulation.
- The study emphasizes the immune balance regulated by TGF-β in early adaptive responses to HBV antigens and context-dependent compensatory mechanisms affecting humoral immunity.