FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2022863994> ?p ?o ?g. }

• W2022863994 endingPage "752" @default.
• W2022863994 startingPage "750" @default.
• W2022863994 abstract "To the Editor: Atopic dermatitis (AD) is a chronic disease usually beginning in childhood. Immunologic features of AD consist in a cytokine balance in the peripheral blood mononuclear cells (PBMC) directed toward Th2 cytokines (Akdis et al., 1997Akdis M. Akdis C.A. Weigl L. Disch R. Blaser K. Skin-homing CLA+ memory T cells are activated in atopic dermatitis and regulate IgE by an IL13-dominated cytokine pattern: IgG4 counter-regulation by CLA-memory T cells.J Immunol. 1997; 159: 4611-4619PubMed Google Scholar;Jirapongsananuruk et al., 1998Jirapongsananuruk O. Hofer M.F. Trumble A.E. Norris D.A. Leung D.Y. Enhanced statement of B7.2 (CD86) in patients with atopic dermatitis: a potential role in the regulation of IgE synthesis.J Immunol. 1998; 160: 4622-4627PubMed Google Scholar). Skin biopsies from atopy patch test (Thepen et al., 1996Thepen T. Langeveld-Wildschut E.G. Bihari I.C. van Wichen D.F. van Reijsen F.C. Mudde G.C. Bruijnzeel-Koomen C.A. Biphasic response against aeroallergen in atopic dermatitis showing a switch from an initial TH2 response to a TH1 response in situ: an immunocytochemical study.J Allergy Clin Immunol. 1996; 97: 828-837Abstract Full Text PDF PubMed Scopus (364) Google Scholar) as well as early phase of spontaneous AD lesions (Hamid et al., 1996Hamid Q. Naseer T. Minshall E.M. Song Y.L. Boguniewicz M. Leung D.Y. In vivo statement of IL-12 and IL-13 in atopic dermatitis.J Allergy Clin Immunol. 1996; 98: 225-231Abstract Full Text Full Text PDF PubMed Scopus (328) Google Scholar) have been shown to bear a mainly Th2 cell infiltrate in contrast to chronic phase spontaneous AD lesions (Hamid et al., 1996Hamid Q. Naseer T. Minshall E.M. Song Y.L. Boguniewicz M. Leung D.Y. In vivo statement of IL-12 and IL-13 in atopic dermatitis.J Allergy Clin Immunol. 1996; 98: 225-231Abstract Full Text Full Text PDF PubMed Scopus (328) Google Scholar), infiltrated by IFN-γ and IL12 expressing mononuclear cells (Grewe et al., 1994Grewe M. Gyufko K. Schöpf E. Krutmann J. Lesional statement of Interferon-gamma in atopic eczema.Lancet. 1994; 343: 25-26Abstract PubMed Scopus (371) Google Scholar;Hamid et al., 1996Hamid Q. Naseer T. Minshall E.M. Song Y.L. Boguniewicz M. Leung D.Y. In vivo statement of IL-12 and IL-13 in atopic dermatitis.J Allergy Clin Immunol. 1996; 98: 225-231Abstract Full Text Full Text PDF PubMed Scopus (328) Google Scholar;Thepen et al., 1996Thepen T. Langeveld-Wildschut E.G. Bihari I.C. van Wichen D.F. van Reijsen F.C. Mudde G.C. Bruijnzeel-Koomen C.A. Biphasic response against aeroallergen in atopic dermatitis showing a switch from an initial TH2 response to a TH1 response in situ: an immunocytochemical study.J Allergy Clin Immunol. 1996; 97: 828-837Abstract Full Text PDF PubMed Scopus (364) Google Scholar). In addition, IL10 is a major cytokine in AD as it is produced in large amounts by PBMC (Ohmen et al., 1995Ohmen J.D. Hanifin J.M. Nickoloff B.J. et al.Overstatement of IL-10 in atopic dermatitis. Contrasting cytokine patterns with delayed-type hypersensitivity reactions.J Immunol. 1995; 154: 1956-1963PubMed Google Scholar;Kallmann et al., 1996Kallmann B.A. Kolb H. Huther M. Martin S. Hellermann M. Lampeter E.F. Interleukine-10 is a predominant cytokine in atopic dermatitis.Arch Dermatol. 1996; 132: 1133-1134Crossref PubMed Scopus (13) Google Scholar) and infiltrating lesional cells of AD patients (Ohmen et al., 1995Ohmen J.D. Hanifin J.M. Nickoloff B.J. et al.Overstatement of IL-10 in atopic dermatitis. Contrasting cytokine patterns with delayed-type hypersensitivity reactions.J Immunol. 1995; 154: 1956-1963PubMed Google Scholar). Recently, the presence of natural killer cells receptors (NKR) on effector T cells has been demonstrated (Lopez-Botet and Bellon, 1999Lopez-Botet M. Bellon T. Natural Killer cell activation and inhibition by receptors for MHC class I.Current Opinion Immunol. 1999; 11: 301-307Crossref PubMed Scopus (141) Google Scholar;Huard and Karlsson, 2000Huard B. Karlsson L. KIR statement on self-reactive CD8+ T cells is controlled by T-cell receptor engagement.Nature. 2000; 403: 325-328https://doi.org/10.1038/35002105.xCrossref PubMed Scopus (0) Google Scholar). The ligands of these receptors are various MHC class I molecules. HLA-G is a nonclassical MHC class I molecule (Carosella et al., 1999Carosella E.D. Rouas-Freiss N. Paul P. Dausset J. HLA-G: a tolerance molecule from the major histocompatibility complex.Immunol Today. 1999; 20: 60-62Abstract Full Text Full Text PDF PubMed Scopus (108) Google Scholar) that has a tissue-restricted expression on extravillous cytotrophoblasts (Mcmaster et al., 1995Mcmaster M.T. Librach C.L. Zhou Y. et al.Human placental HLA-G statement is restricted to differentiated cytotrophoblast.J Immunol. 1995; 154 (3377): 3771PubMed Google Scholar) and thymic epithelial cells (Crisa et al., 1997Crisa L. McMaster M.T. Ishii J.K. Fisher S.J. Salomon D.R. Identification of a thymic epithelial cell subset sharing statement of the class Ib HLA-G molecule with fetal trophoblasts.J Exp Med. 1997; 186: 289-298Crossref PubMed Scopus (260) Google Scholar). Binding studies have shown that one of the ligands of several inhibitory NKR, such as ILT2, ILT4, KIR2DL4, and p49, was indeed HLA-G (Lanier, 1999Lanier L.L. Natural killer cells fertile with receptors for HLA-G?.Proc Natl Acad Sci USA. 1999; 96: 5343-5345Crossref PubMed Scopus (53) Google Scholar). Functionnal assays demonstrated that HLA-G was able to downregulate allogeneic proliferation and cytotoxicity of T cells (Riteau et al., 1999Riteau B. Menier C. Khalil-Daher I. Sedlik C. Dausset J. Rouas-Freiss N. Carosella E.D. HLA-G inhibits the allogeneic proliferation response.J Reprod Immunol. 1999; 43: 203-211Abstract Full Text Full Text PDF PubMed Scopus (161) Google Scholar;Kapasi et al., 2000Kapasi K. Albert S.E. Yie S. Zavazava N. Librach C.L. HLA-G has a concentration-dependent effect on the generation of an allo-CTL response.Immunology. 2000; 101: 191-200https://doi.org/10.1046/j.1365-2567.2000.00109.xCrossref PubMed Scopus (177) Google Scholar), as well as antigen specific T cell cytotoxicity (Le Gal et al., 1999Le Gal F.A. Riteau B. Sedlik C. Khalil-Daher I. et al.HLA-G-mediated inhibition of antigen-specific cytotoxic T lymphocytes.Int Immunol. 1999; 11: 1351-1356Crossref PubMed Scopus (270) Google Scholar) and natural killer cytotoxicity (Rouas-Freiss et al., 1997Rouas-Freiss N. Marchal R.E. Kirszenbaum M. Dausset J. Carosella E.D. The alpha1 domain of HLA-G1 and HLA-G2 inhibits cytotoxicity induced by natural killer cells: is HLA-G the public ligand for natural killer cell inhibitory receptors?.Proc Natl Acad Sci USA. 1997; 94: 5249-5254Crossref PubMed Scopus (316) Google Scholar). HLA-G expression is induced by IL10 (Moreau et al., 1999Moreau P. Adrian-Cabestre F. Menier C. et al.IL-10 selectively induces HLA-G statement in human trophoblasts and monocytes.Int Immunol. 1999; 11: 803-811Crossref PubMed Scopus (350) Google Scholar) or IFN-γ (Yang et al., 1996Yang Y. Chu W. Geragthy D.E. Hunt J.S. statement of HLA-G in human mononuclear Phagocytes and selective induction by IFN-gamma.J Immunol. 1996; 156: 4224-4231PubMed Google Scholar). Because HLA-G may inhibit T cell functions and is induced by a cytokine constantly overexpressed in AD, namely IL10, we studied whether this molecule could be expressed in atopic dermatitis. After local ethical committee approval, adult untreated patients with typical features of AD who gave informed consent were selected. The mean age of the nine included cases was 38.2 y (18–69). Seven of the nine patients had a familial history of atopy and all nine had a long course of AD as the disease began at a mean age of 6 y. The average severity score (SCORAD) at inclusion was 39 (29–63). All biopsies originated from chronic phase AD lesions. As a control, healthy skin was obtained from breast plastic surgery resection. By immunohistochemistry using 87G, a specific antibody for HLA-G (kindly provided by Dan Geraghty, Fred Hutchinson Cancer Reasearch Center, Seattle, WA), HLA-G expressing cells were demonstrated in all nine patients Figure 1. In contrast, 87G never labeled six specimens of healthy skin (data not shown). The density of positive cells was variable from one patient to another. In AD biopsies, HLA-G positive cells were always found in the papillary and less frequently in the reticular dermis; however, in one case there was in addition few epidermal positive cells distributed in all epidermal layers (Figure 1, lower panel). This patient had a very severe disease. In a second step toward determining which cell types expressed HLA-G in AD, we realized double immunofluorescence studies. Using this technique, 87G positive cells appeared to be labeled by anti-CD3 antibodies Figure 2b. Controls consisting of incubation with irrelevant mouse IgG2a, followed by antimouse antibodies conjugated with Texas Red and finally FITC conjugated anti-CD3 antibodies, did not show any double staining Figure 2a, demonstrating that the 87G staining was not due to unspecific binding of the primary or secondary antibody. Using CD14, we were also able to label the HLA-G expressing cells in two out of three patients tested Figure 2c. In the unique patient who had epidermal 87G positive cells, double immunofluorescence also showed few CD1a/HLA-G positive cells Figure 2d. These results show that HLA-G was expressed mainly by T infiltrating cells but also to a lesser extent and less frequently by monocyte-macrophagic or even Langerhans cells. In several situations, HLA-G has been shown to inhibit immune cytotoxicity. Indeed, HLA-G inhibited in vitro T cell proliferation, antigen specific and alloreactive cytotoxicity by interacting with different NKR such as ILT2 (Navarro et al., 1999Navarro F. Llano M. Bellon T. Colonna M. Geraghty D.E. Lopez-Botet M. The ILT2 (LIR1) and CD94/NKG2A NK cell receptors respectively recognize HLA-G1 and HLA-E molecules co-expressed on target cells.Eur J Immunol. 1999; 29: 277-283Crossref PubMed Scopus (293) Google Scholar). In addition, the inhibition of cytotoxicity of maternal decidual natural killer cells against the fetal cytotrophoblast is secondary to the interaction of HLA-G – expressed on cytotrophoblasts – with the NKR expressed on natural killer cells. Similar protection has also been described in some melanoma cell lines in which HLA-G expression has been shown and inhibited natural killer cell cytotoxicity (Paul et al., 1998Paul P. Rouas-Freiss N. Khalil-Daher I. et al.HLA-G expression in melanoma: a way for tumor cells to escape from immunosurveillance.Proc Natl Acad Sci USA. 1998; 95: 4510-4515Crossref PubMed Scopus (374) Google Scholar). Heart transplant recipients who had circulating detectable HLA-G soluble isoforms had less graft rejections than those without peripheral soluble HLA-G (Lila et al., 2000Lila N. Carpentier A. Amrein C. Khalil-Daher I. Dausset J. Carosella E.D. Implication of HLA-G molecule in heart-graft acceptance.Lancet. 2000; 355: 2138Abstract Full Text Full Text PDF PubMed Scopus (193) Google Scholar). In psoriasis, epithelium lining macrophages secrete HLA-G and T infiltrating cells express ILT2 (Aractingi et al, in press). As other authors had previously shown that negative feedback signals were likely to act on psoriatic T infiltrating cells (Nickoloff et al., 1999Nickoloff B.J. Wrone-Smith T. Bonish B. Porcelli S.A. Response of murine and normal human skin to injection of allogeneic blood-derived psoriatic immunocytes: detection of T cells expressing receptors typically present on natural killer cells, including CD94, CD158, and.Cd161 Arch Dermatol. 1999; 135: 546-552Crossref PubMed Scopus (118) Google Scholar), these results strongly suggested that in psoriasis, naturally occurring inhibitory pathways could be mediated at least partly through HLA-G. The results shown herein in AD raise the hypothesis that HLA-G may play a similar role in various chronic inflammatory cutaneous disorders. Furthermore, in AD, T cells have a reduced response to in vitro sensitization procedures even if ex vivo they seem to be activated (Elliot and Hanifin, 1979Elliot S.T. Hanifin J.M. Delayed cutaneous hypersensitivity and lymphocyte transformation: dissociation in atopic dermatitis.Arch Dermatol. 1979; 115: 36-39Crossref PubMed Scopus (67) Google Scholar). In addition, frequent infections may occur in AD patients suggesting decreased local immune response. Therefore, T cells from AD patients may have been the target of negative signals. This could be due to a lack of specific cytotoxic cell activation and/or a lack of antigen processing or presentation (Goodyear et al., 1996Goodyear H.M. McLeish P. Randall S. et al.Immunological studies of herpes simplex virus infection in children with atopic dermatitis.Br J Dermatol. 1996; 134: 85-93Crossref PubMed Scopus (47) Google Scholar). Recently, Cavani et al have shown that antigen specific T regulatory type 1 cells were present in nickel contact dermatitis. These cells mainly expressed IL10 and their supernatants were able to inhibit Th1 cell proliferation as well as dendritic cell maturation specifically induced by nickel (Cavani et al., 2000Cavani A. Nasori F. Prezzi C. Sebastiani S. Albanesi C. Girolomoni G. Human CD4+ T lymphocytes with remarkable regulatory functions on dendritic cells and nickel-specific Th1 immune response.J Invest Dermatol. 2000; 114: 295-302https://doi.org/10.1046/j.1523-1747.2000.00881.xAbstract Full Text Full Text PDF PubMed Scopus (209) Google Scholar). Part of this inhibition was not beared by IL10, suggesting that other signaling factors were implicated. In AD, there is IL10 excess and – as described above – indirect evidence for T and/or antigen presenting cell inhibitory pathways. Because HLA-G was constantly found in AD dermal infiltrate, this molecule may be part of inhibitory pathways implicated in the spontaneously favorable evolutions that may occur in the course of AD as well as in the local observed immunodeficiency. Further studies are needed to establish and understand the role of HLA-G in the course of this disease and the local immunodeficiency." @default.
• W2022863994 created "2016-06-24" @default.
• W2022863994 creator A5022594313 @default.
• W2022863994 creator A5035641630 @default.
• W2022863994 creator A5041378929 @default.
• W2022863994 creator A5061447553 @default.
• W2022863994 creator A5065244911 @default.
• W2022863994 creator A5084151252 @default.
• W2022863994 date "2001-09-01" @default.
• W2022863994 modified "2023-10-12" @default.
• W2022863994 title "HLA-G Expression in Atopic Dermatitis" @default.
• W2022863994 cites W1532423969 @default.
• W2022863994 cites W1612595544 @default.
• W2022863994 cites W1965780550 @default.
• W2022863994 cites W1970074105 @default.
• W2022863994 cites W1976677947 @default.
• W2022863994 cites W2015941743 @default.
• W2022863994 cites W2022275876 @default.
• W2022863994 cites W2044283485 @default.
• W2022863994 cites W2049999044 @default.
• W2022863994 cites W2060648357 @default.
• W2022863994 cites W2070915602 @default.
• W2022863994 cites W2083306286 @default.
• W2022863994 cites W2084278750 @default.
• W2022863994 cites W2084559051 @default.
• W2022863994 cites W2089858271 @default.
• W2022863994 cites W2100279258 @default.
• W2022863994 cites W2102151740 @default.
• W2022863994 cites W2108463809 @default.
• W2022863994 cites W2145110135 @default.
• W2022863994 cites W2160048269 @default.
• W2022863994 cites W4231407601 @default.
• W2022863994 doi "https://doi.org/10.1046/j.0022-202x.2001.01487.x" @default.
• W2022863994 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11564188" @default.
• W2022863994 hasPublicationYear "2001" @default.
• W2022863994 type Work @default.
• W2022863994 sameAs 2022863994 @default.
• W2022863994 citedByCount "72" @default.
• W2022863994 countsByYear W20228639942012 @default.
• W2022863994 countsByYear W20228639942013 @default.
• W2022863994 countsByYear W20228639942014 @default.
• W2022863994 countsByYear W20228639942015 @default.
• W2022863994 countsByYear W20228639942016 @default.
• W2022863994 countsByYear W20228639942017 @default.
• W2022863994 countsByYear W20228639942020 @default.
• W2022863994 countsByYear W20228639942021 @default.
• W2022863994 countsByYear W20228639942022 @default.
• W2022863994 countsByYear W20228639942023 @default.
• W2022863994 crossrefType "journal-article" @default.
• W2022863994 hasAuthorship W2022863994A5022594313 @default.
• W2022863994 hasAuthorship W2022863994A5035641630 @default.
• W2022863994 hasAuthorship W2022863994A5041378929 @default.
• W2022863994 hasAuthorship W2022863994A5061447553 @default.
• W2022863994 hasAuthorship W2022863994A5065244911 @default.
• W2022863994 hasAuthorship W2022863994A5084151252 @default.
• W2022863994 hasBestOaLocation W20228639941 @default.
• W2022863994 hasConcept C147483822 @default.
• W2022863994 hasConcept C16005928 @default.
• W2022863994 hasConcept C188280979 @default.
• W2022863994 hasConcept C203014093 @default.
• W2022863994 hasConcept C2778329239 @default.
• W2022863994 hasConcept C71924100 @default.
• W2022863994 hasConceptScore W2022863994C147483822 @default.
• W2022863994 hasConceptScore W2022863994C16005928 @default.
• W2022863994 hasConceptScore W2022863994C188280979 @default.
• W2022863994 hasConceptScore W2022863994C203014093 @default.
• W2022863994 hasConceptScore W2022863994C2778329239 @default.
• W2022863994 hasConceptScore W2022863994C71924100 @default.
• W2022863994 hasIssue "3" @default.
• W2022863994 hasLocation W20228639941 @default.
• W2022863994 hasLocation W20228639942 @default.
• W2022863994 hasOpenAccess W2022863994 @default.
• W2022863994 hasPrimaryLocation W20228639941 @default.
• W2022863994 hasRelatedWork W1506200166 @default.
• W2022863994 hasRelatedWork W1995515455 @default.
• W2022863994 hasRelatedWork W2048182022 @default.
• W2022863994 hasRelatedWork W2080531066 @default.
• W2022863994 hasRelatedWork W2748952813 @default.
• W2022863994 hasRelatedWork W2899084033 @default.
• W2022863994 hasRelatedWork W3024829390 @default.
• W2022863994 hasRelatedWork W3031052312 @default.
• W2022863994 hasRelatedWork W3032375762 @default.
• W2022863994 hasRelatedWork W3108674512 @default.
• W2022863994 hasVolume "117" @default.
• W2022863994 isParatext "false" @default.
• W2022863994 isRetracted "false" @default.
• W2022863994 magId "2022863994" @default.
• W2022863994 workType "article" @default.