| Literature DB >> 11438456 |
S Aractingi1, N Briand, C Le Danff, M Viguier, H Bachelez, L Michel, L Dubertret, E D Carosella.
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.Entities:
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Year: 2001 PMID: 11438456 PMCID: PMC1850403 DOI: 10.1016/S0002-9440(10)61675-6
Source DB: PubMed Journal: Am J Pathol ISSN: 0002-9440 Impact factor: 4.307