Different regulation of MHC class I antigen processing components in human tumors

J Immunotoxicol. 2008 Oct;5(4):361-7. doi: 10.1080/15476910802482870.


In recent years, progress has been made in understanding how peptides presented by MHC Class I molecules were generated, in particular which proteases are involved in this process and how intracellular pathways influence antigen presentation in professional antigen-presenting cells and various types of tumor cells. This review will give an overview of MHC Class I abnormalities in malignancies and their underlying molecular mechanisms. Dependent on the tumor types structural alterations in particular of the MHC Class I heavy chain, beta(2)-m and the TAP1 subunit have been found at a low frequency, whereas dysregulation of MHC Class I antigen processing components appears to be the major mechanism of MHC Class I down-regulation in tumors of distinct origin. This could occur at the epigenetic, transcriptional and/or post-transcriptional level. The lack or suppression of MHC Class I surface expression due to antigen-processing deficiencies are accompanied by reduced recognition and lysis by antigen-specific cytotoxic T-lymphocytes, which is further often associated with disease progression.

Publication types

  • Review

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B, Member 2
  • ATP-Binding Cassette Transporters / physiology
  • Antigen Presentation / immunology*
  • Down-Regulation / immunology
  • Histocompatibility Antigens Class I / immunology*
  • Humans
  • Neoplasms / immunology*
  • Neoplasms / physiopathology*
  • Peptide Hydrolases / physiology
  • Proteasome Endopeptidase Complex / physiology
  • beta 2-Microglobulin / physiology


  • ATP Binding Cassette Transporter, Subfamily B, Member 2
  • ATP-Binding Cassette Transporters
  • Histocompatibility Antigens Class I
  • TAP1 protein, human
  • beta 2-Microglobulin
  • Peptide Hydrolases
  • Proteasome Endopeptidase Complex