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HLA-E is a Major Ligand for the Natural Killer Inhibitory Receptor CD94/NKG2A
by
Carretero, Marta
, Lopez-Botet, Miguel
, Ishitani, Akiko
, Navarro, Francisco
, Geraghty, Daniel E.
, Lee, Ni
, Llano, Manuel
in
Antibodies
/ Antigens, CD - metabolism
/ Biological Sciences
/ Cell lines
/ Cytotoxicity, Immunologic
/ Dimerization
/ Histocompatibility Antigens Class I - metabolism
/ HLA antigens
/ HLA Antigens - metabolism
/ HLA-E Antigens
/ Humans
/ Immunity
/ Immunity, Cellular
/ Killer Cells, Natural - immunology
/ Lectins, C-Type
/ Ligands
/ Membrane Glycoproteins - metabolism
/ Molecular interactions
/ Molecules
/ Natural killer cells
/ NK Cell Lectin-Like Receptor Subfamily D
/ Peptides - immunology
/ Receptors
/ Receptors, Immunologic - metabolism
/ T lymphocytes
1998
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HLA-E is a Major Ligand for the Natural Killer Inhibitory Receptor CD94/NKG2A
by
Carretero, Marta
, Lopez-Botet, Miguel
, Ishitani, Akiko
, Navarro, Francisco
, Geraghty, Daniel E.
, Lee, Ni
, Llano, Manuel
in
Antibodies
/ Antigens, CD - metabolism
/ Biological Sciences
/ Cell lines
/ Cytotoxicity, Immunologic
/ Dimerization
/ Histocompatibility Antigens Class I - metabolism
/ HLA antigens
/ HLA Antigens - metabolism
/ HLA-E Antigens
/ Humans
/ Immunity
/ Immunity, Cellular
/ Killer Cells, Natural - immunology
/ Lectins, C-Type
/ Ligands
/ Membrane Glycoproteins - metabolism
/ Molecular interactions
/ Molecules
/ Natural killer cells
/ NK Cell Lectin-Like Receptor Subfamily D
/ Peptides - immunology
/ Receptors
/ Receptors, Immunologic - metabolism
/ T lymphocytes
1998
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HLA-E is a Major Ligand for the Natural Killer Inhibitory Receptor CD94/NKG2A
by
Carretero, Marta
, Lopez-Botet, Miguel
, Ishitani, Akiko
, Navarro, Francisco
, Geraghty, Daniel E.
, Lee, Ni
, Llano, Manuel
in
Antibodies
/ Antigens, CD - metabolism
/ Biological Sciences
/ Cell lines
/ Cytotoxicity, Immunologic
/ Dimerization
/ Histocompatibility Antigens Class I - metabolism
/ HLA antigens
/ HLA Antigens - metabolism
/ HLA-E Antigens
/ Humans
/ Immunity
/ Immunity, Cellular
/ Killer Cells, Natural - immunology
/ Lectins, C-Type
/ Ligands
/ Membrane Glycoproteins - metabolism
/ Molecular interactions
/ Molecules
/ Natural killer cells
/ NK Cell Lectin-Like Receptor Subfamily D
/ Peptides - immunology
/ Receptors
/ Receptors, Immunologic - metabolism
/ T lymphocytes
1998
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HLA-E is a Major Ligand for the Natural Killer Inhibitory Receptor CD94/NKG2A
Journal Article
HLA-E is a Major Ligand for the Natural Killer Inhibitory Receptor CD94/NKG2A
1998
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Overview
We previously showed that the availability of a nonamer peptide derived from certain HLA class I signal sequences is a necessary requirement for the stabilization of endogenous HLA-E expression on the surface of 721.221 cells. This led us to examine the ability of HLA-E to protect HLA class I transfectants from natural killer (NK) cell-mediated lysis. It was possible to implicate the CD94/NKG2A complex as an inhibitory receptor recognizing this class Ib molecule by using as target a.221 transfectant selectively expressing surface HLA-E. HLA-E had no apparent inhibitory effect mediated through the identified Ig superfamily (Ig-SF) human killer cell inhibitory receptors or ILT2/LIR1. Further studies of CD94/NKG2+ NK cell-mediated recognition of.221 cells transfected with different HLA class I allotypes (i.e., -Cw4, -Cw3, -B7) confirmed that the inhibitory interaction was mediated by CD94/NKG2A recognizing the surface HLA-E molecule, because only antibodies directed against either HLA-E, CD94, or CD94/NKG2A specifically restored lysis. Surface stabilization of HLA-E in cold-treated.221 cells loaded with appropriate peptides was sufficient to confer protection, resulting from recognition of the HLA class Ib molecule by the CD94/NKG2A inhibitory receptor. Consistent with the prediction that the ligand for CD94/NKG2A is expressed ubiquitously, our examination of HLA-E antigen distribution indicated that it is detectable on the surface of a wide variety of cell types.
Publisher
National Academy of Sciences of the United States of America,National Acad Sciences,The National Academy of Sciences
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