title: Soluble HLA-G molecules impair natural killer/dendritic cell crosstalk via inhibition of dendritic cells.
abstract: HLA-G molecules are known to exert immunosuppressive action on DC maturation and on NK cells, and can in consequence inhibit respectively T cell responses and NK cytolysis. In this study, we show that monocyte-derived DC, differentiated in the presence of GM-CSF and IL-4, are sensitive to soluble (s) HLA-G molecules during LPS/IFN-gamma maturation as demonstrated by the decrease of CD80 and HLA-DR expressions and IL-12 secretion. Moreover, DC pretreated with sHLA-G were found to activate NK/DC crosstalk less than non-treated DC. Early activation of NK cells co-cultured with autologous DC was diminished as assessed by CD69 expression. The IFN-gamma production was impaired whereas a slight inhibition of the NK cell cytotoxicity against Daudi cell line was observed. Since sHLA-G is expressed in grafts or sites of tumour proliferation, its indirect action on NK cells via DC could constitute a pathway of early inhibition for both innate and specific immune responses.
authors.affiliation: UPRES EA 3889, Faculté de Médecine, Université de Rennes 1, Rennes, France.
authors.forename: Frédéric
authors.initials: F
authors.lastname: Gros
authors.forename: Florian
authors.initials: F
authors.lastname: Cabillic
authors.forename: Olivier
authors.initials: O
authors.lastname: Toutirais
authors.forename: Amélie Le
authors.initials: AL
authors.lastname: Maux
authors.forename: Yasmine
authors.initials: Y
authors.lastname: Sebti
authors.forename: Laurence
authors.initials: L
authors.lastname: Amiot
mesh_terms: D015703:Antigens, CD / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D018122:B7-1 Antigen / Q000378:metabolism; D002450:Cell Communication / Q000187:drug effects* / Q000276:immunology; D018920:Coculture Techniques; D003601:Cytotoxicity Tests, Immunologic; D003602:Cytotoxicity, Immunologic / Q000187:drug effects / Q000276:immunology; D003713:Dendritic Cells / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D006680:HLA Antigens / Q000494:pharmacology*; D006684:HLA-DR Antigens / Q000378:metabolism; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I / Q000494:pharmacology*; D006801:Humans; D007155:Immunologic Factors / Q000494:pharmacology; D007371:Interferon-gamma / Q000378:metabolism / Q000494:pharmacology; D018664:Interleukin-12 / Q000378:metabolism; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism; D037181:Lectins, C-Type; D000075362:Leukocyte Immunoglobulin-like Receptor B1; D008070:Lipopolysaccharides / Q000494:pharmacology; D008213:Lymphocyte Activation / Q000187:drug effects; D008562:Membrane Glycoproteins / Q000378:metabolism; D011971:Receptors, Immunologic / Q000378:metabolism; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D018122:B7-1 Antigen; D006680:HLA Antigens; D006684:HLA-DR Antigens; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I; D007155:Immunologic Factors; D007371:Interferon-gamma; D018664:Interleukin-12; D037181:Lectins, C-Type; D000075362:Leukocyte Immunoglobulin-like Receptor B1; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D011971:Receptors, Immunologic; D000099192:CD69 Antigens; C105299:LILRB1 protein, human; C491341:LILRB2 protein, human