title: HLA-G and NK receptor are expressed in psoriatic skin: a possible pathway for regulating infiltrating T cells?
abstract: Recent data have suggested that in psoriasis, the T-infiltrating cells could be submitted to regulatory pathways, possibly through natural killer receptors. HLA-G binds to different natural killer receptors and is able to inhibit T-cell functions. Because this molecule is induced by interferon-gamma, a major cytokine in psoriasis, we asked whether HLA-G and its receptor might be expressed in this disease. Specific RNAs for HLA-G1 and HLA-G5 were consistently found in lesional skin specimens, soluble HLA-G5 transcripts being found only in psoriasis. HLA-G protein was found in all psoriatic sections, but never in normal skin controls. Double labeling demonstrated that HLA-G-positive cells were CD68(+), CD11c(+) macrophages. The NKR ILT2 was also present in psoriatic skin, the T CD4(+)-infiltrating cells expressing indeed ILT2. The demonstration of HLA-G and ILT2 expression in psoriatic skin suggests that this pathway may act as an inhibitory feed back aimed to down-regulate the deleterious effects of T-cell infiltrate in this disease.
authors: SRHI (CEA,DSV-DRM), Commissariat à l'Energie Atomique,Unité de Dermatologie, Paris, France. selim.aractingi@tnn.ap-hop-paris.fr
authors: S
authors: S
authors: Aractingi
authors: N
authors: N
authors: Briand
authors: C
authors: C
authors: Le Danff
authors: M
authors: M
authors: Viguier
authors: H
authors: H
authors: Bachelez
authors: L
authors: L
authors: Michel
authors: L
authors: L
authors: Dubertret
authors: E D
authors: ED
authors: Carosella
mesh_terms: D017398:Alternative Splicing; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism; D005260:Female; D006680:HLA Antigens / Q000235:genetics / Q000378:metabolism* / Q000502:physiology; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I / Q000235:genetics / Q000378:metabolism* / Q000502:physiology; D006801:Humans; D016167:Integrin alphaXbeta2 / Q000378:metabolism; D000075362:Leukocyte Immunoglobulin-like Receptor B1; D016246:Lymphocytes, Tumor-Infiltrating / Q000502:physiology; D008264:Macrophages / Q000378:metabolism; D011565:Psoriasis / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011971:Receptors, Immunologic / Q000378:metabolism* / Q000502:physiology; D012016:Reference Values; D012867:Skin / Q000378:metabolism* / Q000473:pathology; D013601:T-Lymphocytes / Q000502:physiology; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D006680:HLA Antigens; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I; D016167:Integrin alphaXbeta2; D000075362:Leukocyte Immunoglobulin-like Receptor B1; D012333:RNA, Messenger; D011971:Receptors, Immunologic; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C105299:LILRB1 protein, human; C081849:NKTR protein, human