Production of antibody to hepatitis B surface antigen (anti‐HBs) by murine hepatitis B virus carriers: neonatal tolerance versus antigen presentation by dendritic cells

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<jats:p>The inability of hepatitis B virus (HBV) transgenic mice, which express abundant hepatitis B surface antigen (HBsAg) in sera from the neonatal period onwards, to produce antibody to HBsAg (anti‐HBs) is considered to be due to defective function of lymphocytes. The defective function is thought to result from neonatal tolerance because antigenic challenge during the neonatal period is considered to be a tolerogenic event rather than an immunogenic one. However, a series of mixed culture experiments <jats:italic>in vitro</jats:italic> showed that lymphocytes taken from transgenic mice that had been injected with HBsAg in complete Freund’s adjuvant (CFA) constitutively produced anti‐HBs when cultured with dendritic cells from age‐, sex‐ and major histocompatibility complex (MHC)‐matched normal mice, but not when cultured with dendritic cells from transgenic mice. The expression of major histocompatibility complex (MHC) class II and B 7.2 (CD86) antigens on dendritic cells was significantly lower in transgenic mice compared with the same from the normal mice (<jats:italic>P</jats:italic><0·05). Treatment of transgenic mice with interferon‐γ (IFN‐γ) resulted in up‐regulation of MHC class II on dendritic cells, and lymphocytes from HBsAg‐injected transgenic mice produced anti‐HBs <jats:italic>in vitro</jats:italic> when cultured with dendritic cells from IFN‐γ‐treated transgenic mice, but not when cultured with the dendritic cells from untreated transgenic mice. These experiments have shown that defective function of antigen‐presenting cells (APC), not immunogenic tolerance, is responsible for the inability of murine HBV‐carriers to produce anti‐HBs. Production of anti‐HBs by lymphocytes from HBsAg‐injected transgenic mice in the presence of dendritic cells that express higher levels of MHC class II and CD86 antigens has inspired optimism that a more effective vaccine therapy can be developed for chronic HBV‐carriers, injecting vaccine containing HBsAg with modulator(s) of APC function of dendritic cells.</jats:p>

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  • Immunology

    Immunology 92 (4), 494-500, 1997-12

    Wiley

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