315 Scopus citations


Previous studies on NK recognition of HLA-G1 employed as targets 721.221 transfectants (.221-G1) that unknowingly co-expressed the HLA-E molecule, subsequently found to be a major ligand for the CD94/NKG2 receptors. In the present study we re-evaluated the relative role played by CD94/NKG2 and ILT2(LIR1) molecules in recognition of HLA-G1 by NK clones. We employed as targets .221-G1 cells and a surface HLA-E-negative transfectant, .221-G1(E(neg)), generated by site-directed mutagenesis of the HLA-G1 leader sequence. The antagonistic effects of receptor- (ie. CD94/NKG2A, ILT2) and ligand-specific mAb (i.e. HLA-G, HLA-E) were assessed. In addition, binding of an ILT2-lg fusion protein to the .221-AEH, expressing only HLA-E, and the .221-G1(E(neg)) transfectants was analyzed. Our data demon strate that NK recognition of cells expressing HL4-G1 involves at least two non-overlapping receptor-ligand systems: the CD94/NKG2 interaction with HLA-E, and the engagement of the ILT2(LIR1) receptor by HLA-G1 molecules.

Original languageEnglish
Pages (from-to)277-283
Number of pages7
JournalEuropean Journal of Immunology
Issue number1
StatePublished - 1999


  • CD94
  • HLA-E
  • HLA-G
  • NK cell
  • Non-classical MHC


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