Distinct regulation of humoral and cellular immunities to hepatitis B surface antigen.

The surface envelope protein of hepatitis B virus (HBsAg) stimulates the immune system to produce anti-HBs antibodies and to generate cell-mediated immunity. These two arms of immunity were found to be regulated differently in bm12 (H-2bm12) or CBA and C3H (H-2k) mice. In bm12 mutant (I-A beta mutant of B6 mice) mice, the anti-HBs production, early-type, and immune complex-type hypersensitivity were impaired, but the delayed-type hypersensitivity and the T-cell proliferation in vitro were normal compared to the parental B6 (H-2b) mice. The mutation of the A beta molecule seems to affect the immune responses differentially. On the other hand, C3H or CBA mice produced anti-HBs antibodies after major S protein (pre-S-depleted HBsAg) stimulation, but could not generate the hypersensitivity responses. The pre-S region could circumvent the non-responsiveness of the hypersensitivity response in C3H and CBA mice. These data suggest that the humoral and cellular immunities to the HBsAg particle are regulated distinctly and are affected by either the A beta molecule of the host or the pre-S region of the HBsAg.