Mycobacterium tuberculosis inhibits MHC class II antigen processing in murine bone marrow macrophages

Cell Immunol. 2000 Apr 10;201(1):63-74. doi: 10.1006/cimm.2000.1633.


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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antigen Presentation / immunology*
  • Bone Marrow Cells / immunology*
  • Bone Marrow Cells / microbiology
  • HLA-D Antigens / biosynthesis
  • Histocompatibility Antigens Class II / biosynthesis
  • Histocompatibility Antigens Class II / immunology*
  • Macrophages / immunology*
  • Macrophages / microbiology
  • Mice
  • Mice, Inbred CBA
  • Mycobacterium tuberculosis / immunology*


  • H2-M antigens
  • HLA-D Antigens
  • HLA-DM antigens
  • Histocompatibility Antigens Class II
  • I-Ak antigen