title: Skin CD4+ T cells produce interferon-gamma in vitro in response to streptococcal antigens in chronic plaque psoriasis.
abstract: Recently, we have demonstrated that group A streptococcal antigen reactive T cells are present in the skin lesions of chronic plaque psoriasis. To determine the cytokine profile (interferon-gamma, interleukin-4 and interleukin-10) of these T cells in response to streptococcal antigens, T cell lines were cultured from untreated lesional skin of 13 patients with chronic plaque psoriasis and 12 patients with other inflammatory skin diseases. T cell lines were incubated with or without a sonicated heat-killed mixture of group A streptococcal isolates for 18 h in the presence of a transport inhibitor, stained for surface CD4 or CD8 and intracellular cytokine expression, and analyzed by flow cytometry. Psoriatic T cell lines were grown from 10 of 13 patients and were predominately CD4+ (64%-85%) with 10%-32% CD8+ T cells. Variable numbers of CD4+ T cells produced interferon-gamma (0.8%-35%, median 13.9) in eight of 10 T cell lines (p < 0.02). In contrast, CD4+ T cells in five of 12 T cell lines obtained from disease controls did not produce or produced minimal interferon-gamma in response to group A streptococcal isolates; this was significantly different from the psoriatic T cell lines (p < 0.05). Small numbers of interleukin-10 positive (0.8%-1.3%) and interleukin-4 positive (2.1%-2.5%) CD4+ T cells induced by group A streptococcal isolates were also present in two out of five and three out of five psoriatic T cell lines, respectively. This was significantly less in each case than the numbers of CD4+/interferon-gamma+ T cells (p < 0.05). Cytokine-positive CD8+ T cells were rarely observed. These findings demonstrate that a subpopulation of CD4+ T cells in chronic plaque psoriasis skin lesions produces interferon-gamma in response to streptococcal antigens and may be relevant to the pathogenesis of psoriasis.
authors.affiliation: Department of Dermatology, Imperial College School of Medicine at St. Mary's, London, UK.
authors.forename: D W
authors.initials: DW
authors.lastname: Brown
authors.forename: B S
authors.initials: BS
authors.lastname: Baker
authors.forename: J M
authors.initials: JM
authors.lastname: Ovigne
authors.forename: C
authors.initials: C
authors.lastname: Hardman
authors.forename: A V
authors.initials: AV
authors.lastname: Powles
authors.forename: L
authors.initials: L
authors.lastname: Fry
mesh_terms: D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology* / Q000378:metabolism*; D002908:Chronic Disease; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D011565:Psoriasis / Q000276:immunology* / Q000473:pathology*; D012867:Skin / Q000166:cytology* / Q000378:metabolism*; D013194:Staining and Labeling; D013297:Streptococcus pyogenes / Q000276:immunology*
chemical_list: D000942:Antigens, Bacterial; D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma