title: Mast cells and T cells in Kimura's disease express increased levels of interleukin-4, interleukin-5, eotaxin and RANTES.
abstract: BACKGROUND
  Kimura's disease (KD) is a chronic inflammatory disorder characterized by tumours in the head and neck region, enlarged lymph nodes, increased eosinophil counts andhigh serum IgE. Mast cells are known to play a central role in IgE-mediated allergic diseases through the release of inflammatory mediators like IL-4, IL-5 and chemokines. We hypothesized that mast cells may play a role in the pathogenesis of KD by regulating eosinophilic infiltration and IgE synthesis.
  
  
  OBJECTIVE
  In order to investigate the role of mast cells in the pathogenesis of KD, we examined the expression of cytokines/chemokines in the lesions of KD.
  
  
  METHODS
  We examined the number of tryptase+ cells, EG2+ cells, CD3+ cells, IL-4+ cells, IL-5+ cells, eotaxin+ cells, RANTES+ cells and CCR3+ cells in five specimens of KD versus normal tissues by immunohistochemistry. The sources of IL-4, IL-5, eotaxin and RANTES and the expression of CCR3 were examined by immunostaining of serial sections with antibodies to IL-4, IL-5, eotaxin, RANTES and CCR3, and antibodies to tryptase, ECP (EG2) and CD3.
  
  
  RESULTS
  Mast cells, activated eosinophils, T cells, IL-4+ cells, IL-5+ cells, eotaxin+ cells, RANTES+ cells and CCR3+ cells were all increased in the lesions of KD as compared with those in normal tissue. Mast cells and T cells were the major source of IL-4, whereas mast cells, T cells and activated eosinophils were the main source of IL-5. Mast cells, T cells and activated eosinophils were the main source of eotaxin and RANTES.
  
  
  CONCLUSIONS
  The number of IL-4, IL-5, eotaxin and RANTES-expressing mast cells and T cells were increased in the lesions of KD. As mast cells are lesional resident cells, these cells may play an important role in the pathogenesis of KD by regulating IgE synthesis and orchestrating eosinophilic infiltration.
authors.affiliation: Department of Dermatology, Nippon Medical School, Tokyo, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Kimura
authors.forename: R
authors.initials: R
authors.lastname: Pawankar
authors.forename: M
authors.initials: M
authors.lastname: Aoki
authors.forename: Y
authors.initials: Y
authors.lastname: Niimi
authors.forename: S
authors.initials: S
authors.lastname: Kawana
mesh_terms: D000328:Adult; D000796:Angiolymphoid Hyperplasia with Eosinophilia / Q000276:immunology*; D054413:Chemokine CCL11; D018946:Chemokine CCL5 / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism*; D019742:Chemokines, CC / Q000378:metabolism; D004804:Eosinophils / Q000473:pathology; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D015847:Interleukin-4 / Q000378:metabolism; D015848:Interleukin-5 / Q000378:metabolism; D008297:Male; D008407:Mast Cells / Q000276:immunology*; D054397:Receptors, CCR3; D019707:Receptors, Chemokine / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: C515456:CCL11 protein, human; C515350:CCR3 protein, human; D054413:Chemokine CCL11; D018946:Chemokine CCL5; D018925:Chemokines; D019742:Chemokines, CC; D015848:Interleukin-5; D054397:Receptors, CCR3; D019707:Receptors, Chemokine; D015847:Interleukin-4