title: Th1, Th2, Th17 and regulatory T cell pattern in psoriatic patients: modulation of cytokines and gene targets induced by etanercept treatment and correlation with clinical response.
abstract: BACKGROUND
  Psoriasis is sustained by pro-inflammatory CD4+ T helper cells mainly belonging to the Th1, Th17 and Th22 lineage.
  
  
  OBJECTIVE
  To identify whether treatment with the anti-tumour-necrosis-factor antagonist etanercept is able to induce significant modulations in transcription factor and cytokine mRNA gene expressions related to the different T cell immune response polarization (Th1, Th2, Th17 and regulatory T cells, Treg and to correlate them with clinical response.
  
  
  METHODS
  The study population included 19 psoriasis patients treated with etanercept and 19 healthy subjects. Blood samples were collected at baseline and every 4 weeks during treatment. Taqman quantitative real-time polymerase chain reaction was applied to analyse the expression of: Stat-4, T-bet, IL-12p35 and IFN-γ (Th1-related); GATA-3, IL-4 (Th2-related); Stat-3, RORγt, IL-23p19 (Th17-related); Foxp3, IL-2 (Treg-related). Flow cytometry was applied to analyse CD4+CD25+(bright)Foxp3+ cells in peripheral blood.
  
  
  RESULTS
  Upregulation of Th1 and Th17 and downregulation of Treg subsets was found at baseline. The response to etanercept could be associated with a significant reversal of the Th1/Th17 activation, and a concomitant upregulation of Th2 and Treg subsets.
  
  
  CONCLUSIONS
  Our data may contribute to a better understanding of the mechanisms underlying the achievement of clinical response in psoriasis and could be helpful for the identification of early predictive markers of response.
authors.affiliation: Department of Medical Sciences and Human Oncology, Dermatology Section, Turin University, Turin, Italy. pietro.quaglino@unito.it
authors.forename: P
authors.initials: P
authors.lastname: Quaglino
authors.forename: M
authors.initials: M
authors.lastname: Bergallo
authors.forename: R
authors.initials: R
authors.lastname: Ponti
authors.forename: E
authors.initials: E
authors.lastname: Barberio
authors.forename: S
authors.initials: S
authors.lastname: Cicchelli
authors.forename: E
authors.initials: E
authors.lastname: Buffa
authors.forename: A
authors.initials: A
authors.lastname: Comessatti
authors.forename: C
authors.initials: C
authors.lastname: Costa
authors.forename: M E
authors.initials: ME
authors.lastname: Terlizzi
authors.forename: S
authors.initials: S
authors.lastname: Astegiano
authors.forename: M
authors.initials: M
authors.lastname: Novelli
authors.forename: R
authors.initials: R
authors.lastname: Cavallo
authors.forename: M G
authors.initials: MG
authors.lastname: Bernengo
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D016207:Cytokines / Q000235:genetics; D000068800:Etanercept; D005260:Female; D020869:Gene Expression Profiling; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use*; D007155:Immunologic Factors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011565:Psoriasis / Q000188:drug therapy* / Q000276:immunology; D012333:RNA, Messenger / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D050378:T-Lymphocytes, Regulatory / Q000378:metabolism*; D018417:Th1 Cells / Q000378:metabolism*; D058504:Th17 Cells / Q000378:metabolism*; D018418:Th2 Cells / Q000378:metabolism*; D014157:Transcription Factors / Q000378:metabolism; D016896:Treatment Outcome
chemical_list: D016207:Cytokines; D007074:Immunoglobulin G; D007155:Immunologic Factors; D012333:RNA, Messenger; D018124:Receptors, Tumor Necrosis Factor; D014157:Transcription Factors; D000068800:Etanercept