title: Milk-induced urticaria is associated with the expansion of T cells expressing cutaneous lymphocyte antigen.
abstract: BACKGROUND
  Two forms of IgE-mediated skin reactions, atopic dermatitis (AD) and urticaria, have been associated with milk allergy. The reason for these distinct reactions is poorly understood. T cells expressing cutaneous lymphocyte antigen (CLA), a unique skin-homing receptor, are known to play an important role in AD. In contrast, the role of lymphocytes in patients with milk-induced urticaria is unclear.
  
  
  OBJECTIVE
  The expression of the skin-specific homing receptor CLA after in vitro milk protein-specific stimulation was investigated to determine whether T-lymphocyte homing to the skin plays a role in food-induced urticaria.
  
  
  METHODS
  Fourteen patients with milk-induced urticaria but no evidence of AD were included in the study and compared with 6 children with milk-induced AD, 6 children with milk-induced gastrointestinal diseases, and 6 nonatopic and 6 atopic individuals without milk allergy. PBMCs were cultured in the presence or absence of caseins or tetanus toxoid. T-cell proliferation was determined, and T-cell phenotyping was performed by means of flow cytometry with anti-CD4, anti-CD8, and anti-CLA mAbs.
  
  
  RESULTS
  After in vitro stimulation with caseins, PBMCs from patients with milk-induced urticaria and AD had a significantly greater percentage of CD4(+) T cells expressing CLA than patients with milk-induced gastrointestinal symptoms and atopic or nonatopic control subjects. After tetanus stimulation in vitro, no significant difference between the groups was observed. T cells from both patients with milk-induced urticaria and control subjects proliferated well in response to caseins and tetanus.
  
  
  CONCLUSIONS
  Lymphocytes expressing CLA are selectively activated in patients with milk-induced urticaria and may play an important role in the pathogenesis of this disease. Expression of CLA is not unique to milk-induced inflammation in the skin of patients with AD and milk allergy.
authors.affiliation: Division of Pediatric Allergy and Immunology and the Jaffe Institute for Food Allergy, The Mount Sinai School of Medicine, New York 10029-6574, USA.
authors.forename: Kirsten
authors.initials: K
authors.lastname: Beyer
authors.forename: Russell
authors.initials: R
authors.lastname: Castro
authors.forename: Carolyn
authors.initials: C
authors.lastname: Feidel
authors.forename: Hugh A
authors.initials: HA
authors.lastname: Sampson
mesh_terms: D000293:Adolescent; D000328:Adult; D000945:Antigens, Differentiation, T-Lymphocyte; D000951:Antigens, Neoplasm; D002364:Caseins / Q000494:pharmacology; D002478:Cells, Cultured; D002648:Child; D002675:Child, Preschool; D003876:Dermatitis, Atopic / Q000209:etiology; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D007223:Infant; D008213:Lymphocyte Activation; D008562:Membrane Glycoproteins / Q000032:analysis*; D008875:Middle Aged; D016269:Milk Hypersensitivity / Q000150:complications* / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D014581:Urticaria / Q000209:etiology*
chemical_list: D000945:Antigens, Differentiation, T-Lymphocyte; D000951:Antigens, Neoplasm; C063419:CTAGE1 protein, human; D002364:Caseins; D008562:Membrane Glycoproteins; D014409:Tumor Necrosis Factor-alpha; D007073:Immunoglobulin E