title: Influence of in vitro IL-2 or IL-15 alone or in combination with Hsp-70-derived 14-mer peptide (TKD) on the expression of NK cell activatory and inhibitory receptors.
abstract: NK cells represent a potential tool for adoptive immunotherapy against tumors. Membrane-bound Hsp70 acts as a tumor-specific marker enhancing NK cell activity. Using flow cytometry the effect of in vitro stimulation with IL-2 or IL-15 alone or in combination with Hsp70-derived 14-mer peptide (TKD) on cell surface expression of NK activatory receptors (CD16, NKG2D, NKG2C, NKp46, NKp44, NKp30, KIR2DL4, DNAM-1, and LAMP1) and NK inhibitory receptors (NKG2A, KIR2DL2/L3, LIR1/ILT-2, and NKR-P1A) in healthy individuals was studied. Results were expressed as the percentage of receptor expressing cells and the amount of receptor expressed by CD3(-)CD56(+) cellular population. CD94, NKG2D, NKp44, NKp30, KIR2DL4, DNAM-1, LAMP1, NKG2A, and NKR-P1A were upregulated after the stimulation with IL-2 or IL-15 alone or in combination with TKD. KIR2DL2/L3 was upregulated only by IL-15 and IL-15/TKD. Concurrently, an increase in a number of NK cells positive for CD94, NKp44, NKp30, KIR2DL4, and LAMP1 was observed. IL-15 and IL-15/TKD caused also cell number rise positive for KIR2DL2/L3 and NKR-P1A. Cell number positive for NKG2C and NKG2A was increased only by IL-2 and IL-2/TKD. The diverse effect of IL-2 or IL-15 w or w/o TKD on cell surface expression was observed in CD16, NKp46, and LIR1/ILT-2.
authors.affiliation: Department of Molecular Biology and Cell Pathology, Third Faculty of Medicine, Charles University in Prague, Ruska 87, 100 00 Prague, Czech Republic. ilona.hromadnikova@lf3.cuni.cz
authors.forename: Ilona
authors.initials: I
authors.lastname: Hromadnikova
authors.forename: Petra
authors.initials: P
authors.lastname: Pirkova
authors.forename: Lucie
authors.initials: L
authors.lastname: Sedlackova
mesh_terms: D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D002478:Cells, Cultured; D018840:HSP70 Heat-Shock Proteins / Q000737:chemistry*; D006801:Humans; D019409:Interleukin-15 / Q000494:pharmacology*; D007376:Interleukin-2 / Q000494:pharmacology*; D007694:Killer Cells, Natural / Q000187:drug effects* / Q000378:metabolism*; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism; D051907:Lysosomal Membrane Proteins / Q000378:metabolism; D055651:NK Cell Lectin-Like Receptor Subfamily B / Q000378:metabolism; D055654:NK Cell Lectin-Like Receptor Subfamily C / Q000378:metabolism; D055655:NK Cell Lectin-Like Receptor Subfamily K / Q000378:metabolism; D055627:Natural Cytotoxicity Triggering Receptor 1 / Q000378:metabolism; D055629:Natural Cytotoxicity Triggering Receptor 2 / Q000378:metabolism; D055628:Natural Cytotoxicity Triggering Receptor 3 / Q000378:metabolism; D010455:Peptides / Q000737:chemistry* / Q000494:pharmacology*; D017452:Receptors, IgG / Q000378:metabolism; D054343:Receptors, KIR2DL2; D054345:Receptors, KIR2DL4 / Q000378:metabolism; D000098862:T Lineage-Specific Activation Antigen 1; D052118:Lysosomal-Associated Membrane Protein 1
chemical_list: D000945:Antigens, Differentiation, T-Lymphocyte; D018840:HSP70 Heat-Shock Proteins; D019409:Interleukin-15; D007376:Interleukin-2; D051907:Lysosomal Membrane Proteins; D055651:NK Cell Lectin-Like Receptor Subfamily B; D055654:NK Cell Lectin-Like Receptor Subfamily C; D055655:NK Cell Lectin-Like Receptor Subfamily K; D055627:Natural Cytotoxicity Triggering Receptor 1; D055629:Natural Cytotoxicity Triggering Receptor 2; D055628:Natural Cytotoxicity Triggering Receptor 3; D010455:Peptides; D017452:Receptors, IgG; D054343:Receptors, KIR2DL2; D054345:Receptors, KIR2DL4; D000098862:T Lineage-Specific Activation Antigen 1; C515077:KIR2DL2 protein, human; C515079:KIR2DL4 protein, human; C527203:KLRB1 protein, human; C527059:KLRC2 protein, human; C527085:KLRK1 protein, human; C489116:LAMP1 protein, human; D052118:Lysosomal-Associated Membrane Protein 1; C112260:NCR1 protein, human; C112837:NCR2 protein, human; C431710:NCR3 protein, human