Immune interferon activates multiple class II major histocompatibility complex genes and the associated invariant chain gene in human endothelial cells and dermal fibroblasts

T. Collins, A. J. Korman, C. T. Wake, J. M. Boss, D. J. Kappes, W. Fiers, K. A. Ault, M. A. Gimbrone, J. L. Strominger, J. S. Pober

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498 Scopus citations

Abstract

Immune interferon (IFN-γ) increases the surface expression of HLA-A,B antigens and induces the surface expression of HLA-DR antigens on vascular endothelial cells and dermal fibroblasts. Here we report that IFN-γ induces parallel expression of two other class II major histocompatibility complex (MHC) antigens, SB and DC. Maximal surface expression of all three antigens is reached in 4-6 days, and HLA-DR and -SB are induced to a higher level of expression than HLA-DC. For all three class II antigens, induction is marked by the de novo appearance of detectable transcripts of class II heavy and light chains and of the non-MHC-encoded invariant chain, suggestive of the transcription of multiple previously silent genes. Class I message levels and antigen expression are also increased by IFN-γ at similar rates but from initial levels that are 50% of maximal. After removal of IFN-γ, class II antigen expression persists for at least 4 days, while mRNA levels decrease rapidly. The parallel induction and persistence of the several class II MHC antigens may be important in conferring immune accessory function on vascular and stromal cells.

Original languageEnglish
Pages (from-to)4917-4921
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume81
Issue number15
DOIs
StatePublished - 1984

Keywords

  • Endothelium/physiology
  • Gene Expression Regulation/drug effects
  • Genes
  • HLA-DP Antigens
  • HLA-DQ Antigens
  • HLA-DR Antigens
  • Histocompatibility Antigens Class II/genetics
  • Humans
  • Interferon-gamma/immunology
  • Macromolecular Substances
  • Major Histocompatibility Complex
  • RNA, Messenger/genetics
  • Skin/cytology
  • Transcription, Genetic/drug effects

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