title: Proliferation and release of IL-5 and IFN-gamma by peripheral blood mononuclear cells from cat-allergic asthmatics and rhinitics, non-cat-allergic asthmatics, and normal controls to peptides derived from Fel d 1 chain 1.
abstract: BACKGROUND
  In general, T cells from normal, nonatopic individuals respond to aeroallergens with synthesis and release of IFN-gamma. In contrast, release of T(H)2-type cytokines by activated lymphocytes is a feature of allergic rhinitis and atopic asthma.
  
  
  OBJECTIVE
  The purpose of this study was to determine differences in T-cell recognition of epitopes within allergenic sequences, in terms of proliferation and cytokine production, in subjects with atopic asthma compared with subjects with allergic rhinitis and normal controls.
  
  
  METHODS
  Proliferative responses and IL-5/IFN-gamma release patterns from PBMCs from cat-allergic asthmatic, cat-allergic rhinitic, and non-cat-allergic asthmatic subjects and nonatopic normal controls were determined in primary cultures. Cells were challenged with 7 overlapping peptides spanning chain 1 of the major cat allergen, Fel d 1.
  
  
  RESULTS
  The 4 groups did not differ with respect to the ability to mount proliferative responses to Fel d 1 peptides. In all groups, the IFN-gamma responses were predominantly to the amino terminus peptides. Cat-allergic and non-cat-allergic asthmatic subjects (and not cat-allergic rhinitic subjects and normal controls) made IL-5 responses to most of the Fel d 1 peptides, the result being a mixed (T(H)0) cytokine response at the N-terminus and a restricted (T(H)2) response at the C-terminus.
  
  
  CONCLUSIONS
  Proliferative and IL-5/IFN-gamma responses of T cells from asthmatic and atopic rhinitic subjects and normal controls to allergen peptides can be dissociated. Furthermore, differing cytokine responses to peptides derived from a single antigen suggest that certain domains of the molecule might preferentially induce IL-5 rather than IFN-gamma and as a result could be more important in disease pathogenesis.
authors.affiliation: Department of Allergy and Clinical Immunology, Imperial College School of Medicine at the National Heart and Lung Institute, London, United Kingdom.
authors.forename: B M
authors.initials: BM
authors.lastname: Haselden
authors.forename: E
authors.initials: E
authors.lastname: Syrigou
authors.forename: M
authors.initials: M
authors.lastname: Jones
authors.forename: D
authors.initials: D
authors.lastname: Huston
authors.forename: K
authors.initials: K
authors.lastname: Ichikawa
authors.forename: M D
authors.initials: MD
authors.lastname: Chapman
authors.forename: A B
authors.initials: AB
authors.lastname: Kay
authors.forename: M
authors.initials: M
authors.lastname: Larché
mesh_terms: D000328:Adult; D000485:Allergens / Q000276:immunology*; D000818:Animals; D001249:Asthma / Q000276:immunology*; D002415:Cats; D000939:Epitopes / Q000276:immunology; D005260:Female; D006023:Glycoproteins / Q000276:immunology*; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology; D007371:Interferon-gamma / Q000378:metabolism*; D015848:Interleukin-5 / Q000378:metabolism*; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000276:immunology; D012220:Rhinitis / Q000276:immunology; D006377:T-Lymphocytes, Helper-Inducer
chemical_list: D000485:Allergens; D000939:Epitopes; D006023:Glycoproteins; D015848:Interleukin-5; D010446:Peptide Fragments; D007371:Interferon-gamma; C059296:Fel d 1 protein, Felis domesticus