title: Engagement of natural cytotoxicity programs regulates AP-1 expression in the NKL human NK cell line.
abstract: NK cell cytotoxicity is a fast and efficient mechanism of target cell lysis. Using transcription analysis, such as multiplex messenger assays, we show here that natural cytotoxicity exerted by the human NKL cell line correlates with mRNA accumulation of very early activator protein (AP)-1 transcription factor genes such as JunB, FosB and c-Fos. In addition, DNA-binding activities of Jun-Fos heterodimers were observed by electrophoretic mobility shift assays during the course of natural cytotoxicity. Interaction between immunoglobulin-like transcript-2/leukocyte Ig-like receptor 1 on NKL cells and HLA-B27 on target cells leads to an impairment of NKL natural cytotoxicity, which correlates with an absence of JunB, FosB, and c-Fos transcription, as well as an absence of their DNA-binding activity. Our studies thus indicate that, despite the rapidity of NK cell-mediated lysis, AP-1 transcription factor is activated during the early stage of NK cell cytolytic programs and that engagement of NK cell inhibitory receptors for MHC class I molecules impairs the very early activation of AP-1.
authors: Centre d'Immunologie, Institut National de la Santé et de la Recherche Médicale (INSERM)/Centre National de la Recherche Scientifique (CNRS) de Marseille-Luminy, France.
authors: K
authors: K
authors: Bernard
authors: A
authors: A
authors: Cambiaggi
authors: S
authors: S
authors: Guia
authors: F
authors: F
authors: Bertucci
authors: S
authors: S
authors: Granjeaud
authors: R
authors: R
authors: Tagett
authors: C
authors: C
authors: N'Guyen
authors: B R
authors: BR
authors: Jordan
authors: E
authors: E
authors: Vivier
mesh_terms: D015703:Antigens, CD / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D002460:Cell Line; D003602:Cytotoxicity, Immunologic / Q000235:genetics* / Q000276:immunology; D004247:DNA / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000276:immunology; D016762:Genes, fos / Q000235:genetics; D016758:Genes, jun / Q000235:genetics; D015235:HLA-B Antigens / Q000276:immunology; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism; D037181:Lectins, C-Type; D000075362:Leukocyte Immunoglobulin-like Receptor B1; D009693:Nucleic Acid Hybridization / Q000235:genetics / Q000379:methods; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D016755:Proto-Oncogene Proteins c-jun / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011971:Receptors, Immunologic / Q000276:immunology; D018808:Transcription Factor AP-1 / Q000096:biosynthesis* / Q000235:genetics; D015854:Up-Regulation / Q000235:genetics / Q000276:immunology; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D004247:DNA; D015235:HLA-B Antigens; D037181:Lectins, C-Type; D000075362:Leukocyte Immunoglobulin-like Receptor B1; D016760:Proto-Oncogene Proteins c-fos; D016755:Proto-Oncogene Proteins c-jun; D012333:RNA, Messenger; D011971:Receptors, Immunologic; D018808:Transcription Factor AP-1; D000099192:CD69 Antigens; C105299:LILRB1 protein, human