title: Immunologic Overlap of Helper T-Cell Subtypes 17 and 22 in Erythrodermic Psoriasis and Atopic Dermatitis.
abstract: OBJECTIVE
  Psoriasis and atopic dermatitis (AD) are inflammatory diseases thought to be mediated by helper T-cell subtypes 1 and 2 (TH1 and TH2), respectively. Although psoriasis and AD show histopathologic differences during chronic disease, they are difficult to distinguish histologically during erythrodermic exacerbations.
  
  
  OBJECTIVE
  To determine whether the immune phenotype of helper T cells can differentiate erythrodermic psoriasis and erythrodermic AD by studying skin biopsy specimens of patients with psoriasis and AD during erythrodermic and chronic disease phases.
  
  
  METHODS
  We conducted a retrospective study using biopsy samples of psoriasis, AD, and erythroderma belonging to the surgical pathology files of the James Homer Wright Pathology Laboratories, Massachusetts General Hospital, and collected from January 1, 2004, through December 31, 2011. Samples were obtained from patients with chronic psoriasis (n = 20), chronic AD (n = 20), erythroderma subsequently diagnosed as psoriasis (n = 7), and erythroderma subsequently diagnosed as AD (n = 5). We evaluated immunohistochemical stains for CD3 and dual stains for CD4 and T-bet, GATA binding protein 3 (GATA3), signal transducer and activator of transcription 3 (STAT3), or basonuclin 2 (BNC2), which are transcription factors reported to be specific and mutually exclusive for TH1, TH2, TH17, and TH22 cells, respectively. Two investigators independently counted CD3+ cells and dual-labeled CD4+/T-bet+, CD4+/GATA3+, CD4+/STAT3+, and CD4+/BNC2+ cells in 5 consecutive high-power fields.
  
  
  METHODS
  We evaluated the percentage of TH1, TH2, TH17, and TH22 cells in CD3+ T cells and the TH1:TH2 ratio in chronic psoriasis, chronic AD, erythrodermic psoriasis, and erythrodermic AD.
  
  
  RESULTS
  We found a significant difference in the TH1:TH2 ratio between chronic psoriasis and chronic AD (0.26 and 0.09, respectively; P = .005). However, we detected no significant difference in the percentage of TH1 (6.5% and 4.8%), TH2 (55.2% and 64.6%), TH17 (14.7% and 30.4%), and TH22 (3.8% and 3.3%) cells of CD3+ T cells or in the TH1:TH2 ratio (0.16 and 0.07) within biopsy specimens from patients with erythrodermic psoriasis and AD, respectively.
  
  
  CONCLUSIONS
  This study confirms the TH1- and TH2-skewed phenotype of chronic psoriasis and chronic AD, respectively. However, the immune phenotype, as determined by immunohistochemical analysis, cannot discriminate between these inflammatory diseases in the erythrodermic phase. These findings advance our understanding of the pathophysiological characteristics of erythroderma, psoriasis, and AD and may influence therapeutic decisions.
authors.affiliation: Pathology Service, Dermatopathology Unit, Massachusetts General Hospital and Harvard Medical School, Boston.
authors.forename: Andrea Primiani
authors.initials: AP
authors.lastname: Moy
authors.affiliation: Pathology Service, Dermatopathology Unit, Massachusetts General Hospital and Harvard Medical School, Boston2Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston.
authors.forename: Mandakolathur
authors.initials: M
authors.lastname: Murali
authors.affiliation: Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Boston.
authors.forename: Daniela
authors.initials: D
authors.lastname: Kroshinsky
authors.affiliation: Pathology Service, Dermatopathology Unit, Massachusetts General Hospital and Harvard Medical School, Boston.
authors.forename: Lyn M
authors.initials: LM
authors.lastname: Duncan
authors.affiliation: Pathology Service, Dermatopathology Unit, Massachusetts General Hospital and Harvard Medical School, Boston.
authors.forename: Rosalynn M
authors.initials: RM
authors.lastname: Nazarian
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D017252:CD3 Complex / Q000032:analysis; D015704:CD4 Antigens / Q000032:analysis; D004268:DNA-Binding Proteins / Q000032:analysis; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000473:pathology; D003873:Dermatitis, Exfoliative / Q000276:immunology* / Q000473:pathology; D005260:Female; D050990:GATA3 Transcription Factor / Q000032:analysis; D006801:Humans; D007150:Immunohistochemistry; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D011565:Psoriasis / Q000276:immunology* / Q000473:pathology; D012189:Retrospective Studies; D050796:STAT3 Transcription Factor / Q000032:analysis; D020825:T-Box Domain Proteins / Q000032:analysis; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology / Q000473:pathology; D058504:Th17 Cells / Q000276:immunology / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology / Q000473:pathology; D055815:Young Adult; D000098815:T-bet Transcription Factor
chemical_list: C484527:BNC2 protein, human; D017252:CD3 Complex; D015704:CD4 Antigens; D004268:DNA-Binding Proteins; D050990:GATA3 Transcription Factor; C494749:GATA3 protein, human; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D020825:T-Box Domain Proteins; D000098815:T-bet Transcription Factor