Cytokines increase transporter in antigen processing-1 expression more rapidly than HLA class I expression in endothelial cells

J Immunol. 1992 Nov 15;149(10):3297-301.

Abstract

Transporter in Ag processing-1 (TAP-1, previously called PSF-1 or Ring-4) is an MHC-encoded gene product that is required for efficient association of intracellular peptide Ag with nascent HLA class I H chain and beta 2-microglobulin, thereby permitting assembly and normal surface expression of the class I molecules. TAP-1 is thought to function as a component of a transmembrane pump, that transports cytoplasmically-derived peptides into the lumen of the endoplasmic reticulum where class I molecules assemble. Synthesis and expression of HLA class I molecules is increased in human endothelial cells by IFN-beta, IFN-gamma, and TNF. We report these same cytokines increase TAP-1 expression. As with class I, TAP-1 is also synergistically increased by combinations of TNF with IFN. Interestingly, cytokine-induced increases in TAP-1 mRNA are markedly more rapid than increases in class I mRNA. This rapid increase in TAP-1 mRNA is reflected in a rapid increase in TAP-1 protein. These results demonstrate that TAP-1 synthesis and class I synthesis are regulated in parallel. The rapidity of the cytokine response of TAP-1 compared to class I further suggests that the constitutive level of TAP-1 expression in endothelial cells is not sufficient to support inducible increases in class I expression.

Publication types

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

MeSH terms

  • Animals
  • Carrier Proteins / biosynthesis*
  • Carrier Proteins / genetics
  • Cells, Cultured
  • Endothelium, Vascular / metabolism*
  • Histocompatibility Antigens Class I / biosynthesis*
  • Histocompatibility Antigens Class I / genetics
  • Humans
  • Interferons / pharmacology*
  • Mice
  • Protein Biosynthesis / drug effects
  • RNA, Messenger / analysis
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Carrier Proteins
  • Histocompatibility Antigens Class I
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Interferons