| pubmed-article:6780914 | pubmed:abstractText | BCG can either act as an adjuvant to potentiate immunological responses or, in some cases, can induce suppression. The reasons for these differential activities are not clear but may include routes and doses of administration, as well as variable host reactivity to the agent. In this study, we have used killed BCG administered intravenously to produce chronic granulomatous inflammation (CGI) in the lungs and spleen of inbred mice. We report that strains which develop CGI were usually anergic, as evaluated by the development of delayed hypersensitivity (DH) to sheep erythrocytes (SRBC). Studies on the genetics of BCG-induced anergy indicated that it was unigenic, recessive and linked (approximately 28 recombination units) to the immunoglobulin heavy-chain allotype (Igh). There was no influence by genes linked to the major histocompatibility complex. The study indicates that anergy associated with CGI is under genetic control, which may explain the variability of anergy in patients with granulomatous diseases. The implication of linkage to the Igh complex is not clear, but it may be associated with VH receptors on T lymphocytes, which in turn act on macrophages to mediate suppression. | lld:pubmed |
