Legionella pneumophila down-regulates MHC class I expression of human monocytic host cells and thereby inhibits T cell activation

Cell Mol Life Sci. 2005 Mar;62(5):578-88. doi: 10.1007/s00018-005-4518-4.


Legionella (L.) pneumophila, the causative agent of Legionnaires' disease, is an intracellular pathogen of alveolar macrophages that resides in a compartment displaying features of endoplasmatic reticulum (ER). In this study, we show that intracellular multiplication of L. pneumophila results in a remarkable decrease in MHC class I expression by the infected monocytes. During intracellular multiplication, L. pneumophila absorbs ER-resident chaperons such as calnexin and BiP, molecules that are required for the correct formation of the MHC class I complex. Due to reduced MHC class I expression, stimulation of allogeneic blood mononuclear cells was severely inhibited by infected host cells but cytotoxicity of autologous natural killer cells against Legionella-infected monocytes was not enhanced. Thus, reduced expression of MHC class I in infected monocytes may resemble a new immune escape mechanism induced by L. pneumophila.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Calnexin / analysis
  • Calnexin / metabolism
  • Cytotoxicity, Immunologic / physiology
  • Down-Regulation*
  • Endoplasmic Reticulum / metabolism
  • Endoplasmic Reticulum / microbiology
  • Endoplasmic Reticulum Chaperone BiP
  • Heat-Shock Proteins / analysis
  • Heat-Shock Proteins / metabolism
  • Histocompatibility Antigens Class I / metabolism*
  • Humans
  • Immune Tolerance
  • Interferon-gamma / immunology
  • Interleukin-2 / immunology
  • Killer Cells, Natural / immunology
  • Legionella pneumophila / pathogenicity*
  • Lymphocyte Activation / immunology
  • Molecular Chaperones / analysis
  • Molecular Chaperones / metabolism
  • Monocytes / immunology*
  • Monocytes / microbiology*
  • T-Lymphocytes / immunology*


  • Endoplasmic Reticulum Chaperone BiP
  • Heat-Shock Proteins
  • Histocompatibility Antigens Class I
  • Interleukin-2
  • Molecular Chaperones
  • Calnexin
  • Interferon-gamma