Journal
CELLULAR IMMUNOLOGY
Volume 201, Issue 1, Pages 63-74Publisher
ACADEMIC PRESS INC
DOI: 10.1006/cimm.2000.1633
Keywords
antigen processing; antigen presentation; MHC; monocytes/macrophages; mycobacteria; infectious immunity
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Funding
- NIAID NIH HHS [AI34343, AI27243, AI35726] Funding Source: Medline
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Infection of murine bone-marrow-derived macrophages with viable Mycobacterium tuberculosis (MTB) H37Ra inhibited surface expression of MHC class II (MHC-II) molecules and processing of exogenous antigens for presentation to CD4(+) T hybridoma cells. The inhibition was not dependent on bacterial viability, since it was also produced by exposure to dead bacilli and MTB cytosol preparations, suggesting that it was initiated by a constitutively expressed bacterial component. Northern blot analysis demonstrated that MTB bacilli or cytosol decreased MHC-II mRNA and immunoprecipitation of biosynthetically labeled molecules confirmed that MHC-II protein synthesis was diminished. Exposure to MTB or MTB cytosol also decreased expression of H2-DM, but H2-DM expression was still sufficient to catalyze conversion of MHC-II to SDS-stable dimers, a measure of MHC-II peptide loading. Thus, infection with MTB decreased both MHC-II and H2-DM expression, but diminished MHC-II synthesis provided the major limitation to antigen processing. (C) 2000 Academic Press.
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