title: Allergen-specific responses of CD19(high) and CD19(low) B Cells in Non-IgE-mediated food allergy of late eczematous reactions in atopic dermatitis: presence of IL-17- and IL-32-producing regulatory B cells (Br17 & Br32).
abstract: BACKGROUND
  Food allergies are important etiologic factors in atopic dermatitis. CD19 is a B-cell-specific cell-surface molecule, with a critical role in B-cell activation. Recently, B cells showed independent two subpopulations as CD19(high) and CD19(low). The allergen-specific responses of the CD19(high) and CD19(low) B-cell subpopulations were investigated in patients with non-IgE-mediated food allergy.
  
  
  METHODS
  Five milk-allergic subjects and eight milk-tolerant subjects were selected by a double-blind placebo-controlled food challenge. Peripheral blood mononuclear cells (PBMCs) were stimulated in vitro with casein or ovalbumin and stained with monoclonal antibodies to distinguish the B-cell subsets.
  
  
  RESULTS
  After allergen stimulation, CD19(high) B cells increased in the number and the fraction in PBMCs in the milk-tolerant group, whereas those remained unchanged in the milk-allergic group. These responses were constant, regardless of the kind of food allergen (milk or egg). The resulting CD19(high)/CD19(low) B-cell ratio increased markedly in the milk-tolerant group after allergen stimulation, but was unchanged in the milk-allergic group. IL-10, IL-17, IL-32 and TGF-β- producing regulatory B cells and Foxp3-expressing regulatory B cells were identified predominantly on CD19 low and CD5(+) B cells.
  
  
  CONCLUSIONS
  The response of the CD19(high) B-cell subpopulation to allergen stimulation is decisive for immune tolerance of non-IgE-mediated food allergy in atopic dermatitis. CD19 high and CD5(+) B cells dominantly produce cytokines and express Foxp3. Especially, IL-17 and IL-32 expressing B cells (Br17 & Br32) are present. The exact immunological role of CD19 and cytokines including IL-17 and IL-32 around B cells in immune tolerance requires further investigation.
authors.affiliation: Department of Animal Biotechnology, College of Animal Bioscience & Technology, Konkuk University, Seoul, Korea. admyth@naver.com
authors.forename: Joonyong
authors.initials: J
authors.lastname: Noh
authors.forename: Geunwoong
authors.initials: G
authors.lastname: Noh
mesh_terms: D000293:Adolescent; D000485:Allergens / Q000276:immunology*; D000818:Animals; D018941:Antigens, CD19 / Q000276:immunology*; D016175:B-Lymphocyte Subsets / Q000276:immunology; D018956:CD5 Antigens / Q000276:immunology; D003876:Dermatitis, Atopic / Q000276:immunology*; D004311:Double-Blind Method; D004485:Eczema / Q000276:immunology*; D005260:Female; D005512:Food Hypersensitivity / Q000276:immunology*; D051858:Forkhead Transcription Factors / Q000276:immunology; D006801:Humans; D007108:Immune Tolerance / Q000276:immunology; D007073:Immunoglobulin E / Q000276:immunology; D016753:Interleukin-10 / Q000276:immunology; D020381:Interleukin-17 / Q000276:immunology*; D007378:Interleukins / Q000276:immunology*; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D008892:Milk / Q000276:immunology; D016212:Transforming Growth Factor beta / Q000276:immunology
chemical_list: D000485:Allergens; D018941:Antigens, CD19; D018956:CD5 Antigens; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; C496971:IL32 protein, human; D020381:Interleukin-17; D007378:Interleukins; D016212:Transforming Growth Factor beta; D016753:Interleukin-10; D007073:Immunoglobulin E