Regulation of I-A expression by murine peritoneal macrophages: differences linked to the Bcg gene.

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Abstract
We previously reported that Mycobacterium bovis (strain BCG) induces continuous I-A expression when injected into BCG-resistant strains of mice. We have extended this observation by showing that Corynebacterium parvum also induces continuous I-A expression by macrophages from BCG-resistant but not BCG-susceptible mice. We have linked continuous expression to BCG resistance by using C.D2Ityr mice, which are congenic with BCG-susceptible BALB/c mice except for genes on a portion of chromosome 1, which contains the gene(s) for BCG resistance. Macrophages from C.D2Ityr mice continuously expressed I-A, whereas macrophages from BALB/c mice transiently expressed I-A. Continuous expression by macrophages from both Bcgr and Bcgs mice could be induced in vitro with rIFN-gamma. However, the continuous expression of I-A by macrophages from Bcgs mice required the continued presence of IFN-gamma, whereas that by Bcgr macrophages did not. The continuous expression of I-A by macrophages from Bcgs mice was also inhibited by hydrocortisone, cyclohexamide, tunicamycin, and monensin, whereas I-A expression by Bcgr macrophages was not affected. The continuous expression of I-A by macrophages from Bcgr mice did not require its continued synthesis. The significance of these findings to the induction of immunity and to antimicrobial resistance are discussed.

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