Igh allotype-linked control of immune complex-type hypersensitivity induced by hepatitis B surface antigen.

Hepatitis B surface antigen (HBsAg) induced an immune complex-type hypersensitivity which developed at 5-6 hr after the challenge and could be transferred by anti-HBs antisera, in addition to the delayed-type hypersensitivity in B10.BR mice. The pre-S region of HBsAg influenced this induction because the pre-S-depleted HBsAg or recombinant major S protein could not stimulate this 5-hr ear swelling. The male B10.BR mice responded better than the female ones, probably due to the inhibition by female hormone. Furthermore, HBsAg could also induce an early-occurring hypersensitivity which appeared within 1 hr of the antigen challenge. However, B10.BR mice did not exhibit this hypersensitivity; B6 mice expressed all three types of hypersensitivity (1 hr, 5 hr and 24 hr) and BALB/c mice showed only 1-hr and 24-hr responses. The expression of the immune complex-type seems to be determined by the Ighb gene or gene(s) closely associated to it. Mice bearing the Igh-1b allotype could be stimulated by HBsAg to induce the immune-complex type hypersensitivity. Moreover, it was the high specific binding not the titre of anti-HBs antibodies that influenced the exhibition of immune complex-type hypersensitivity.