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NKG 2C, HLA ‐E and their association with psoriasis
Author(s) -
Patel Forum,
Marusina Alina I.,
Duong Christopher,
Adamopoulos Iannis E.,
Maverakis Emanual
Publication year - 2013
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.12280
Subject(s) - psoriasis , human leukocyte antigen , immunology , major histocompatibility complex , t cell receptor , receptor , mhc class i , biology , hla g , t cell , immune system , genetics , antigen
Natural killer ( NK ) cell activation is regulated by the integration of signals from inhibitory and activating cell surface receptors. Both NKG 2A and NKG 2C pair with CD 94 to form inhibitory and activating receptors specific for the HLA ‐E‐canonical peptide complex. HLA ‐E is a non‐classical MHC class Ib molecule with limited polymorphism. It preferentially binds to and presents leader sequence peptides derived from classical MHC class I molecules. Wilson et al. have identified an association between NKG 2C deficiency and psoriasis. They have also discovered an HLA ‐C‐dependent association between HLA ‐E and psoriasis. Their research highlights the importance of NK cells in the pathophysiology of psoriasis. Herein, we propose two different models to explain the association between NKG 2C, HLA ‐E and psoriasis. In the first model, we hypothesize that NKG 2C deficiency and/or HLA ‐E O1:01 can inhibit the ability of NK cells to regulate autoreactive T cells, predisposing to psoriasis. The second model proposes that HLA ‐E 01:03 can disrupt the presentation of the psoriasis‐inducing self‐determinant by HLA ‐C, thereby protecting against psoriasis.