Inhibitory Killer Immunoglobulin-like receptors to self HLA-B and HLA-C ligands contribute differentially to Natural Killer cell functional potential in HIV infected slow progressors

Inhibitory Killer Immunoglobulin-like Receptors (iKIR) interact with their ligands, HLA molecules, to license Natural Killer (NK) cells for functional competence. Previous studies stimulating peripheral blood mononuclear cells (PBMCs) with the HLA-devoid K562 cell line revealed that NK cells from in...

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Published in	Clinical immunology (Orlando, Fla.) Vol. 143; no. 3; pp. 246 - 255
Main Authors	Kamya, Philomena, Tallon, Benjamin, Melendez-Pena, Carlos, Parsons, Matthew S., Migueles, Stephen A., Connors, Mark, Miconiatis, Sofia, Song, Rujun, Boulet, Salix, Bruneau, Julie, Tremblay, Cecile L., Bernard, Nicole F.
Format	Journal Article
Language	English
Published	Amsterdam Elsevier Inc 01.06.2012 Elsevier
Subjects	Adult Aged Allergy and Immunology Biological and medical sciences CD4 Lymphocyte Count Degranulation Female Fundamental and applied biological sciences. Psychology Fundamental immunology gamma -Interferon Histocompatibility antigen HLA HIV Infections - immunology HLA-B Antigens - immunology HLA-C Antigens - immunology HLA-ligands Human immunodeficiency virus Human viral diseases Humans Immunodeficiencies Immunodeficiencies. Immunoglobulinopathies Immunoglobulin-like receptors Immunopathology Infectious diseases K562 Cells Killer Cells, Natural - immunology Killer-Immunoglobulin-like Receptors Medical sciences Middle Aged Natural Killer (NK) cells Natural killer cells NK function Peripheral blood mononuclear cells Potassium channels (inwardly-rectifying) Receptors, KIR - immunology Self Substance P Tumor necrosis factor- alpha Viral diseases Viral diseases of the lymphoid tissue and the blood. Aids Young Adult Killer-Immunoglobulin-like Receptors Natural Killer (NK) cells NK function HLA-ligands Immunopathology HLA-System Immunoglobulins Ligand Major histocompatibility system Killer immunoglobulin like receptor HLA-C-Locus AIDS Killer-Immunoglobulin-like Immune deficiency Infection Natural killer cell Receptors Immunology Viral disease T-Lymphocyte Class I histocompatibility antigen HLA-B-Locus Biological receptor
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ISSN	1521-6616 1521-7035 1521-7035
DOI	10.1016/j.clim.2012.01.001

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Abstract	Inhibitory Killer Immunoglobulin-like Receptors (iKIR) interact with their ligands, HLA molecules, to license Natural Killer (NK) cells for functional competence. Previous studies stimulating peripheral blood mononuclear cells (PBMCs) with the HLA-devoid K562 cell line revealed that NK cells from individuals with an iKIR encoded by the KIR3DL1 locus with self HLA-Bw4 as their ligands, had higher frequencies of tri-functional NK cells that expressed the degranulation marker CD107a and secreted Interferon-γ and Tumor Necrosis Factor-α than those from individuals who were homozygous for HLA-Bw6 alleles, which are not ligands for these iKIR. To assess the effect of other iKIR to self-HLA (S-iKIR) on the NK cell response, we compared HIV-infected slow progressors (SP) carrying S-iKIR to HLA-C alleles with or without S-iKIR to HLA-Bw4. We show that S-iKIR to HLA-B and C alleles differ in their contribution to NK cell functional potential in HIV-infected SP upon stimulation with K562 targets. ► HLA antigens bind inhibitory Killer immunoglobulin-like receptors (iKIR). ► HLA and iKIR interact to license NK cells for functional competence. ► The impact of iKIR to self HLA-B and C was compared in HIV+ and HIV- subjects. ► S-iKIR to HLA-C contribute little to NK function in HIV infected slow progressors. ► S-iKIR to both HLA-B and HLA-C contribute to NK function in uninfected subjects.
AbstractList	Inhibitory Killer Immunoglobulin-like Receptors (iKIR) interact with their ligands, HLA molecules, to license Natural Killer (NK) cells for functional competence. Previous studies stimulating peripheral blood mononuclear cells (PBMCs) with the HLA-devoid K562 cell line revealed that NK cells from individuals with an iKIR encoded by the KIR3DL1 locus with self HLA-Bw4 as their ligands, had higher frequencies of tri-functional NK cells that expressed the degranulation marker CD107a and secreted Interferon-γ and Tumor Necrosis Factor-α than those from individuals who were homozygous for HLA-Bw6 alleles, which are not ligands for these iKIR. To assess the effect of other iKIR to self-HLA (S-iKIR) on the NK cell response, we compared HIV-infected slow progressors (SP) carrying S-iKIR to HLA-C alleles with or without S-iKIR to HLA-Bw4. We show that S-iKIR to HLA-B and C alleles differ in their contribution to NK cell functional potential in HIV-infected SP upon stimulation with K562 targets. ► HLA antigens bind inhibitory Killer immunoglobulin-like receptors (iKIR). ► HLA and iKIR interact to license NK cells for functional competence. ► The impact of iKIR to self HLA-B and C was compared in HIV+ and HIV- subjects. ► S-iKIR to HLA-C contribute little to NK function in HIV infected slow progressors. ► S-iKIR to both HLA-B and HLA-C contribute to NK function in uninfected subjects. Inhibitory Killer Immunoglobulin-like Receptors (iKIR) interact with their ligands, HLA molecules, to license Natural Killer (NK) cells for functional competence. Previous studies stimulating peripheral blood mononuclear cells (PBMCs) with the HLA-devoid K562 cell line revealed that NK cells from individuals with an iKIR encoded by the KIR3DL1 locus with self HLA-Bw4 as their ligands, had higher frequencies of tri-functional NK cells that expressed the degranulation marker CD107a and secreted Interferon-γ and Tumor Necrosis Factor-α than those from individuals who were homozygous for HLA-Bw6 alleles, which are not ligands for these iKIR. To assess the effect of other iKIR to self-HLA (S-iKIR) on the NK cell response, we compared HIV-infected slow progressors (SP) carrying S-iKIR to HLA-C alleles with or without S-iKIR to HLA-Bw4. We show that S-iKIR to HLA-B and C alleles differ in their contribution to NK cell functional potential in HIV-infected SP upon stimulation with K562 targets.Inhibitory Killer Immunoglobulin-like Receptors (iKIR) interact with their ligands, HLA molecules, to license Natural Killer (NK) cells for functional competence. Previous studies stimulating peripheral blood mononuclear cells (PBMCs) with the HLA-devoid K562 cell line revealed that NK cells from individuals with an iKIR encoded by the KIR3DL1 locus with self HLA-Bw4 as their ligands, had higher frequencies of tri-functional NK cells that expressed the degranulation marker CD107a and secreted Interferon-γ and Tumor Necrosis Factor-α than those from individuals who were homozygous for HLA-Bw6 alleles, which are not ligands for these iKIR. To assess the effect of other iKIR to self-HLA (S-iKIR) on the NK cell response, we compared HIV-infected slow progressors (SP) carrying S-iKIR to HLA-C alleles with or without S-iKIR to HLA-Bw4. We show that S-iKIR to HLA-B and C alleles differ in their contribution to NK cell functional potential in HIV-infected SP upon stimulation with K562 targets. Abstract Inhibitory Killer Immunoglobulin-like Receptors (iKIR) interact with their ligands, HLA molecules, to license Natural Killer (NK) cells for functional competence. Previous studies stimulating peripheral blood mononuclear cells (PBMCs) with the HLA-devoid K562 cell line revealed that NK cells from individuals with an iKIR encoded by the KIR3DL1 locus with self HLA-Bw4 as their ligands, had higher frequencies of tri-functional NK cells that expressed the degranulation marker CD107a and secreted Interferon-γ and Tumor Necrosis Factor-α than those from individuals who were homozygous for HLA-Bw6 alleles, which are not ligands for these iKIR. To assess the effect of other iKIR to self-HLA (S-iKIR) on the NK cell response, we compared HIV-infected slow progressors (SP) carrying S-iKIR to HLA-C alleles with or without S-iKIR to HLA-Bw4. We show that S-iKIR to HLA-B and C alleles differ in their contribution to NK cell functional potential in HIV-infected SP upon stimulation with K562 targets. Inhibitory Killer Immunoglobulin-like Receptors (iKIR) interact with their ligands, HLA molecules, to license Natural Killer (NK) cells for functional competence. Previous studies stimulating peripheral blood mononuclear cells (PBMCs) with the HLA-devoid K562 cell line revealed that NK cells from individuals with an iKIR encoded by the KIR3DL1 locus with self HLA-Bw4 as their ligands, had higher frequencies of tri-functional NK cells that expressed the degranulation marker CD107a and secreted Interferon-γ and Tumor Necrosis Factor-α than those from individuals who were homozygous for HLA-Bw6 alleles, which are not ligands for these iKIR. To assess the effect of other iKIR to self-HLA (S-iKIR) on the NK cell response, we compared HIV-infected slow progressors (SP) carrying S-iKIR to HLA-C alleles with or without S-iKIR to HLA-Bw4. We show that S-iKIR to HLA-B and C alleles differ in their contribution to NK cell functional potential in HIV-infected SP upon stimulation with K562 targets. Inhibitory Killer Immunoglobulin-like Receptors (iKIR) interact with their ligands, HLA molecules, to license Natural Killer (NK) cells for functional competence. Previous studies stimulating peripheral blood mononuclear cells (PBMCs) with the HLA-devoid K562 cell line revealed that NK cells from individuals with an iKIR encoded by the KIR3DL1 locus with self HLA-Bw4 as their ligands, had higher frequencies of tri-functional NK cells that expressed the degranulation marker CD107a and secreted Interferon- gamma and Tumor Necrosis Factor- alpha than those from individuals who were homozygous for HLA-Bw6 alleles, which are not ligands for these iKIR. To assess the effect of other iKIR to self-HLA (S-iKIR) on the NK cell response, we compared HIV-infected slow progressors (SP) carrying S-iKIR to HLA-C alleles with or without S-iKIR to HLA-Bw4. We show that S-iKIR to HLA-B and C alleles differ in their contribution to NK cell functional potential in HIV-infected SP upon stimulation with K562 targets.
Author	Song, Rujun Kamya, Philomena Parsons, Matthew S. Boulet, Salix Migueles, Stephen A. Connors, Mark Tremblay, Cecile L. Bernard, Nicole F. Miconiatis, Sofia Tallon, Benjamin Melendez-Pena, Carlos Bruneau, Julie
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Keywords	Killer-Immunoglobulin-like Receptors Natural Killer (NK) cells NK function HLA-ligands Immunopathology HLA-System Immunoglobulins Ligand Major histocompatibility system Killer immunoglobulin like receptor HLA-C-Locus AIDS Killer-Immunoglobulin-like Immune deficiency Infection Natural killer cell Receptors Immunology Viral disease T-Lymphocyte Class I histocompatibility antigen HLA-B-Locus Biological receptor
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Snippet	Inhibitory Killer Immunoglobulin-like Receptors (iKIR) interact with their ligands, HLA molecules, to license Natural Killer (NK) cells for functional... Abstract Inhibitory Killer Immunoglobulin-like Receptors (iKIR) interact with their ligands, HLA molecules, to license Natural Killer (NK) cells for functional...
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SubjectTerms	Adult Aged Allergy and Immunology Biological and medical sciences CD4 Lymphocyte Count Degranulation Female Fundamental and applied biological sciences. Psychology Fundamental immunology gamma -Interferon Histocompatibility antigen HLA HIV Infections - immunology HLA-B Antigens - immunology HLA-C Antigens - immunology HLA-ligands Human immunodeficiency virus Human viral diseases Humans Immunodeficiencies Immunodeficiencies. Immunoglobulinopathies Immunoglobulin-like receptors Immunopathology Infectious diseases K562 Cells Killer Cells, Natural - immunology Killer-Immunoglobulin-like Receptors Medical sciences Middle Aged Natural Killer (NK) cells Natural killer cells NK function Peripheral blood mononuclear cells Potassium channels (inwardly-rectifying) Receptors, KIR - immunology Self Substance P Tumor necrosis factor- alpha Viral diseases Viral diseases of the lymphoid tissue and the blood. Aids Young Adult
Title	Inhibitory Killer Immunoglobulin-like receptors to self HLA-B and HLA-C ligands contribute differentially to Natural Killer cell functional potential in HIV infected slow progressors
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