Lack of gene complementation prevents expression of I-Ek in recombinant A.TFR5

W. P. Lafuse, J. F. McCormick, C. S. David

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

The I-E molecule is produced by complementation of genes in I-A (A(e)) and I-E (E(α)). Ia specificities 22 and 23 are generated by the hybrid molecule, whereas Ia.7 is an allotypic determinant presumably on the α-chain of the I-E molecule. Recombinant A.TFR5 (A(f)E(k)) lacks detectable I-E molecule since A(f) and E(k) cannot complement. In a cross between A.TFR5 and B10.A(4R) (A(k)E(b)), A(k)(e) and E(k)(α) can succesfully complement to express the I-E(k) molecule on the cell surface of the heterozygote. Haplotypes H-2(b) and H-2(s) can also provide the permissive A(b)(e) and A(s)(e) for complementation with E(k)(α) of A.TFR5.

Original languageEnglish (US)
Pages (from-to)2511-2513
Number of pages3
JournalJournal of Immunology
Volume124
Issue number5
StatePublished - Jan 1 1980

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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    Lafuse, W. P., McCormick, J. F., & David, C. S. (1980). Lack of gene complementation prevents expression of I-Ek in recombinant A.TFR5. Journal of Immunology, 124(5), 2511-2513.