NDLI: Class I-induced resistance to natural killing: identification of nonpermissive residues in HLA-A2.

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Class I-induced resistance to natural killing: identification of nonpermissive residues in HLA-A2.

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Class I-induced resistance to natural killing: identification of nonpermissive residues in HLA-A2.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Dawson, J. R. Storkus, W. J. Ward, F. E. Cresswell, P. Ruiz, R. E. Salter, R. D. Alexander, J.
Description	Author Affiliation: Storkus WJ ( Department of Microbiology, Duke University Medical Center, Durham, NC 27710.);
Abstract	Structural characteristics of major histocompatibility complex class I antigens associated with natural killer (NK)-resistance phenomena were examined. Previous research has shown that transfection of class I genomic DNA clones into class I-deficient, NK-sensitive target cell lines results in transfectants exhibiting class I+, NK-resistant phenotypes. In contrast to the HLA-A3, -B7, -B27, and -Bw58 class I molecules, the HLA-A2 class I molecules were shown not to protect target cells from NK activity. Here we show that this nonprotective phenotype maps to the alpha 1 domain of the HLA-A2 molecule by examining the NK-protective capacity of the natural interdomain recombinant HLA-Aw69 molecule. HLA-Aw69, which consists of an alpha 1 domain exhibiting homology with HLA-Aw68, and alpha 2/alpha 3/transmembrane-cytoplasmic domains, exhibiting homologies with HLA-A2, mimics HLA-Aw68 and provides HLA-A,B null target cell (C1R) transfectants with increased resistance to NK. Further, the inability of transfected HLA-A2 to confer protection against NK activity can be completely attributed to the expression of a 'nonpermissive' residue at position 74 in the alpha 1 domain. Site-directed mutation of the His-74 residue in HLA-A2 to the Asp-74 (HLA-A3, -Aw68, -Aw69, -B7) residue generates a mutant that provides C1R cell line transfectants an NK-resistant phenotype. As His-74 blocks access to a side pocket in the HLA-A2 antigen-binding cleft, these results support the critical involvement of residues within the peptide-binding groove of class I molecules in determining the NK susceptibility phenotype of class I+ target cells.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	14
Volume Number	88
Language	English
Publisher	National Academy of Sciences
Publisher Date	1991-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cytotoxicity, Immunologic HLA-A2 Antigen Immunology Histocompatibility Antigens Class I Killer Cells, Natural Alleles Antibodies, Monoclonal Cell Line Cloning, Molecular Fluorescent Antibody Technique Genetics Histocompatibility Testing Mutagenesis, Site-Directed Phenotype Plasmids Radioimmunoassay Transfection Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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