title: Contrasting patterns of streptococcal superantigen-induced T-cell proliferation in guttate vs. chronic plaque psoriasis.
abstract: BACKGROUND
  Streptococcal infection is strongly associated with guttate psoriasis (GP) and may also exacerbate chronic plaque psoriasis (CPP), possibly through the release of superantigenic toxins.
  
  
  OBJECTIVE
  To investigate superantigen-induced generation of cutaneous lymphocyte associated antigen (CLA) -positive lymphocytes in GP compared with CPP.
  
  
  METHODS
  Peripheral blood lymphocyte (PBL) expression of CLA and T-cell receptor Vbeta chain was assessed in patients with CPP and with active and resolved GP. Expression of superantigen-reactive Vbeta families was compared with in vitro superantigen-induced peripheral blood mononuclear cell (PBMC) proliferation.
  
  
  RESULTS
  Peripheral blood mononuclear cells from patients with active GP showed a twofold increased proliferation after stimulation with streptococcal pyogenic toxins A and streptococcal pyogenic toxins C compared with controls (P < 0.01), whereas the response to the staphylococcal toxins and mitogenic stimulation was the same in all groups. Peripheral blood lymphocytes (PBL) from patients with active GP showed increased use of the superantigen-reactive families Vbeta2 (P < 0.01) and Vbeta17 (P < 0.05), which was not evident in the other patient groups or controls. This pattern of Vbeta expression was only observed in CLA-positive T cells. Furthermore, there was a positive correlation between Vbeta2 expression and enhanced proliferation after stimulation with SPEA (r = 0.82, P < 0.01) and SPEC (r = 0.74, P < 0.05) in active GP.
  
  
  CONCLUSIONS
  This study supports the concept that streptococcal infection precipitates acute GP at least in part through superantigen driven generation of Vbeta-restricted CLA-positive skin homing lymphocytes, whereas we could find no evidence for a similar mechanism occurring in the maintenance of stable CPP.
authors.affiliation: St John's Institute of Dermatology, King's College London, UK.
authors.forename: S C
authors.initials: SC
authors.lastname: Davison
authors.forename: M H
authors.initials: MH
authors.lastname: Allen
authors.forename: E
authors.initials: E
authors.lastname: Mallon
authors.forename: J N
authors.initials: JN
authors.lastname: Barker
mesh_terms: D000328:Adult; D000942:Antigens, Bacterial / Q000276:immunology*; D000943:Antigens, Differentiation / Q000276:immunology*; D001427:Bacterial Toxins / Q000494:pharmacology; D016022:Case-Control Studies; D002455:Cell Division; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000502:physiology; D016131:Lymphocyte Subsets / Q000502:physiology; D008297:Male; D011565:Psoriasis / Q000276:immunology*; D018709:Statistics, Nonparametric; D013290:Streptococcal Infections / Q000276:immunology*; D013291:Streptococcus / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology / Q000502:physiology*
chemical_list: D000942:Antigens, Bacterial; D000943:Antigens, Differentiation; D001427:Bacterial Toxins