title: Increased expression of the natural killer cell inhibitory receptor CD94/NKG2A and CD158b on circulating and lesional T cells in patients with chronic plaque psoriasis.
abstract: BACKGROUND
  Psoriasis is a common inflammatory cutaneous disorder characterized by activated T-cell infiltration. T lymphocytes bearing natural killer cell receptors (NKRs) have been suggested to play an important role in the pathogenesis of psoriasis. However, the expression pattern of activating and inhibitory NKRs on T lymphocytes from psoriatic patients and its significance in psoriasis needs further study.
  
  
  OBJECTIVE
  To investigate the pathogenesis of NKR-expressing T cells in psoriasis.
  
  
  METHODS
  Thirty patients with chronic plaque psoriasis and 20 healthy controls were enrolled in this study. The immunophenotypic profiles of NKRs, including CD56, CD16 (activating NKRs), CD158a, CD158b, CD94 and NKG2A (inhibitory NKRs), were analysed in peripheral blood T lymphocytes, as well as psoriatic lesional infiltrating T cells, by triple-fluorescence flow cytometry.
  
  
  RESULTS
  A significant increase of inhibitory CD8+ CD158b+, CD4 CD8 CD158b+ and CD8+ CD94/NKG2A+ T cells was found in the peripheral blood of patients with psoriasis when compared with controls. Tissue-infiltrating T lymphocytes expressing inhibitory receptors CD158b, CD94 and NKG2A were found in psoriatic lesions. There was a significant positive correlation between the increased percentage of circulating CD8+ CD94/NKG2A+ T cells and the Psoriasis Area and Severity Index.
  
  
  CONCLUSIONS
  In the present study, we demonstrated increased proportions of particular subsets of inhibitory CD158b+ and/or CD94/NKG2A+ T cells in patients with psoriasis. The elevation of these inhibitory NKR-expressing T cells was correlated with disease severity, which may signify the possibility of chronic antigen-driven stimulation and dysregulated cytokine production in the pathogenesis of psoriasis.
authors.affiliation: Department of Obsterics and Gynecology, National Taiwan University Hospital, National Taiwan University College of Medicine, 7, Chung-Shan South Road, Taipei 100, Taiwan.
authors.forename: Y H
authors.initials: YH
authors.lastname: Liao
authors.forename: S H
authors.initials: SH
authors.lastname: Jee
authors.forename: B C
authors.initials: BC
authors.lastname: Sheu
authors.forename: Y L
authors.initials: YL
authors.lastname: Huang
authors.forename: M P
authors.initials: MP
authors.lastname: Tseng
authors.forename: S M
authors.initials: SM
authors.lastname: Hsu
authors.forename: T-F
authors.initials: TF
authors.lastname: Tsai
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D051920:NK Cell Lectin-Like Receptor Subfamily D / Q000097:blood / Q000378:metabolism*; D011565:Psoriasis / Q000097:blood / Q000276:immunology*; D011971:Receptors, Immunologic / Q000097:blood / Q000378:metabolism*; D054340:Receptors, KIR; D054342:Receptors, KIR2DL1; D054344:Receptors, KIR2DL3; D012720:Severity of Illness Index; D012867:Skin / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology*
chemical_list: D051920:NK Cell Lectin-Like Receptor Subfamily D; D011971:Receptors, Immunologic; D054340:Receptors, KIR; D054342:Receptors, KIR2DL1; D054344:Receptors, KIR2DL3