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Down regulation of Qa gene expression on drug-modified tumor cells.

AbstractBACKGROUND:
Mouse leukemia, L1210, strongly enhances its immunogenicity following in vivo treatment with 5-(3-3'-dimethyl-1-triazeno) imidazole-4-carboxamide (DTIC). Previous experiments have shown that transformed cells elicit a cell-mediated response accountable for rejection and resistance to a subsequent injection of parental tumor into a syngeneic host. L1210 expresses classical H-2 class I molecules, and since it has been shown that DTIC treatment does not modify the expression of these molecules, this is a suitable model to study nonclassical class I antigens, such as Qa2 glycoproteins, and their potential role in tumorigenicity.
METHODS:
Cloned cells from L1210 were treated with DTIC and then H-2D, and Qa antigen expression was studied on four clones, before and after xenogenization with DTIC.
RESULTS AND CONCLUSIONS:
a strong decrease of Qa2 molecule expression was demonstrated by radioimmunoassay and immunofluorescent staining and was confirmed by FACS and 2D-gel analysis. The presence or the absence of Qa antigens on tumor cells could thus be involved in tolerance or rejection of tumor cells in syngeneic animals.
AuthorsE Leroy, D Lattuada, C Casnici, P Franco, O E Marelli
JournalTumori (Tumori) Vol. 79 Issue 6 Pg. 439-43 (Dec 31 1993) ISSN: 0300-8916 [Print] United States
PMID8171747 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Dacarbazine
Topics
  • Animals
  • Dacarbazine (pharmacology)
  • Down-Regulation
  • Female
  • Fluorescent Antibody Technique
  • Gene Expression Regulation, Leukemic (drug effects)
  • Genes, MHC Class I (drug effects)
  • Leukemia L1210 (genetics, immunology)
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred DBA
  • Tumor Cells, Cultured

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