title: Identification of a Th2- and Th17-skewed immune phenotype in chronic urticaria with Th22 reduction dependent on autoimmunity and thyroid disease markers.
abstract: BACKGROUND
  Chronic urticaria is a condition with many inciting factors and often presents a therapeutic challenge to clinicians. In addition to a central role for mast cells, an immune dysregulated state related to cytokine/chemokine alterations is increasingly being recognized.
  
  
  METHODS
  Biopsies of chronic urticaria (n = 11) and normal skin (n = 5) were evaluated with immunostains for CD117, CD3 and dual stains for CD4/T-bet, GATA-3, STAT-3 or BNC-2 (transcription factors specific and mutually exclusive for Th1, Th2, Th17 and Th22 cells, respectively). Clinical data, including autoantibodies and thyroid function tests, and the number of CD117+ mast cells and percent of Th1, Th2, Th17 and Th22 of CD3+ T-cells were compared.
  
  
  RESULTS
  Th2 cells and Th17 cells were significantly more frequent in chronic urticaria than controls. In contrast, there was no significant difference in mast cells, Th1 cells or Th22 cells. Three of nine chronic urticaria patients had evidence of autoimmune disease; biopsies from these patients trended toward a greater number of mast cells and decreased percent of Th-cell subtypes as compared with those without autoimmunity markers, with significantly less Th22 cells.
  
  
  CONCLUSIONS
  These findings provide novel insight into the role of Th2 and Th17 in chronic urticaria pathophysiology and may impact therapy.
authors.affiliation: Pathology Service, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
authors.forename: Andrea P
authors.initials: AP
authors.lastname: Moy
authors.affiliation: Pathology Service, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.|Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
authors.forename: Mandakolathur
authors.initials: M
authors.lastname: Murali
authors.affiliation: Pathology Service, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
authors.forename: Rosalynn M
authors.initials: RM
authors.lastname: Nazarian
mesh_terms: D000328:Adult; D000943:Antigens, Differentiation / Q000276:immunology; D001327:Autoimmune Diseases / Q000276:immunology / Q000473:pathology; D002908:Chronic Disease; D005260:Female; D006801:Humans; D008297:Male; D008407:Mast Cells / Q000276:immunology / Q000473:pathology; D008875:Middle Aged; D012189:Retrospective Studies; D012867:Skin / Q000276:immunology / Q000473:pathology; D058504:Th17 Cells / Q000276:immunology / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology / Q000473:pathology; D013959:Thyroid Diseases / Q000276:immunology / Q000473:pathology; D014581:Urticaria / Q000276:immunology / Q000473:pathology
chemical_list: D000943:Antigens, Differentiation
keywords: T lymphocytes; Th cell; immunology; urticaria