Molecular analysis of deficient class I H-2 antigen expression by mouse lung carcinoma cells

J Immunol. 1988 Jun 1;140(11):4003-12.

Abstract

We have continued our investigations of line lung carcinoma cells to understand the molecular basis of decreased expression of class I H-2 Ag and class I Ag induction with DMSO. We show that line 1, a murine lung carcinoma cell line, has low levels of class I Ag (H-2K, D, and L) because it is deficient in both class I and beta 2-microglobulin (B2M) RNA, and that these mRNA can be coordinately induced with DMSO. Evidence presented herein also shows that IFN-gamma can induce surface expression of class I Ag and suggests that it may act through a different mechanism than DMSO in inducing class I Ag. To further evaluate the regulation of class I expression, H-2Dp genes were transfected into line 1 cells. The transfected H-2 genes appear to be constitutively expressed at much higher levels than are the endogenous class I genes because surface expression of the foreign Dp Ag on the transfectants is elevated relative to the endogenous H-2d haplotype class I Ag. Both Dp surface expression and Dp mRNA are induced after treatment with DMSO. In all the Dp transfectants, we observed higher constitutive levels of class I mRNA as well as increased constitutive levels of endogenous B2M mRNA when compared to control or untransfected line 1 cells, however, we could not correlate these constitutive levels with Dp copy number. These results suggest that the regulation of class I and B2M genes is linked and that expression of class I genes can affect the expression of B2M genes.

Publication types

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

MeSH terms

  • Animals
  • Carcinoma / genetics*
  • Carcinoma / immunology
  • Carcinoma / metabolism
  • Cell Line
  • Dimethyl Sulfoxide / pharmacology
  • Genes, MHC Class I / drug effects
  • H-2 Antigens / biosynthesis*
  • H-2 Antigens / genetics
  • Immunologic Deficiency Syndromes / genetics*
  • Immunologic Deficiency Syndromes / metabolism
  • Interferon-gamma / pharmacology
  • Lung Neoplasms / genetics*
  • Lung Neoplasms / immunology
  • Lung Neoplasms / metabolism
  • Mice
  • Mice, Inbred BALB C
  • RNA / biosynthesis
  • RNA, Messenger / metabolism
  • Transfection / drug effects
  • beta 2-Microglobulin / genetics

Substances

  • H-2 Antigens
  • RNA, Messenger
  • beta 2-Microglobulin
  • RNA
  • Interferon-gamma
  • Dimethyl Sulfoxide