Aberrant expression of Fas ligand in mice deficient for the MHC class II transactivator

J Immunol. 2002 May 1;168(9):4414-9. doi: 10.4049/jimmunol.168.9.4414.

Abstract

The MHC class II transactivator (CIITA) is a critical regulator of MHC class II genes and other genes involved in the Ag presentation pathway. CIITA-deficient mice lack MHC class II expression on almost all APCs. In this study, we show that these mice also have aberrant Fas ligand expression on both CD4 T cells and B cells. We found that Fas ligand expression was greatly increased on CIITA-deficient CD4 T cells during the Th1 differentiation process. However, both CIITA-deficient and control Th1 effector cells up-regulated Fas ligand to similar levels if cells were reactivated. The introduction of CIITA into primary CD4 T cells via retroviral infection resulted in a reduction in the level of Fas ligand and delay in apoptosis after activation. Interestingly, activated B cells from the CIITA-deficient mice also showed increased levels of Fas ligand that could be to some degree inhibited by the introduction of IL-4.

Publication types

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

MeSH terms

  • Animals
  • Apoptosis
  • B-Lymphocytes / immunology*
  • Cell Differentiation
  • Cells, Cultured
  • Fas Ligand Protein
  • Humans
  • Jurkat Cells
  • Kinetics
  • Membrane Glycoproteins / genetics
  • Membrane Glycoproteins / metabolism*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Nuclear Proteins*
  • RNA, Messenger / biosynthesis
  • Th1 Cells / immunology*
  • Trans-Activators / genetics
  • Trans-Activators / physiology*
  • Transcriptional Activation

Substances

  • FASLG protein, human
  • Fas Ligand Protein
  • Fasl protein, mouse
  • MHC class II transactivator protein
  • Membrane Glycoproteins
  • Nuclear Proteins
  • RNA, Messenger
  • Trans-Activators