title: Expression of eotaxin, interleukin 13 and tumour necrosis factor-alpha in dermatitis herpetiformis.
abstract: BACKGROUND
  The dermal and perivascular infiltrate in dermatitis herpetiformis (DH), which is mainly composed of CD4+ lymphocytes, neutrophils and eosinophils, is believed to play an important part in the pathogenesis of the disease. Previous studies suggest that cytokines such as interleukin (IL) -8, granulocyte-macrophage colony-stimulating factor, IL-4 and IL-5 could be involved in the pathogenesis of DH. These cytokines appear to drive tissue infiltration and maturation of eosinophils. Part of the effect of T-helper (Th) 2-type cytokines (IL-4, IL-5) on eosinophils could be mediated by eotaxin, which is a highly specific chemotactic protein induced by various cytokines [IL-4, IL-13, tumour necrosis factor (TNF) -alpha and interferon-gamma].
  
  
  OBJECTIVE
  To evaluate the expression of eotaxin and its inducers, IL-13 and TNF-alpha, in DH. METHODS We examined lesions collected from 10 DH patients with active disease. Sections from each specimen were incubated with anti-IL-13, anti-TNF-alpha and anti-eotaxin antibodies. Chloroacetyl esterase reaction was performed to show mast cell infiltration.
  
  
  RESULTS
  Eotaxin was mainly expressed at the tips of the dermal papillae, within the microabscesses. Positivity was also found in the lymphomonocytic infiltrate in the dermis. IL-13 was expressed in the dermal infiltrate and TNF-alpha was found in the inflammatory infiltrate and in dermal vascular cells.
  
  
  CONCLUSIONS
  These findings confirm the importance of the lymphomonocytic infiltrate and of Th2 cytokines in the pathogenesis of this disease, suggesting that tissue infiltration in DH is mediated by cell-specific chemokines such as eotaxin and not only by non-specific chemokines such as IL-8.
authors.affiliation: Departments of Dermatology and Pathology, University of Ancona, Ancona, Italy. p.amerio@idi.it
authors.forename: P
authors.initials: P
authors.lastname: Amerio
authors.forename: R
authors.initials: R
authors.lastname: Verdolini
authors.forename: M
authors.initials: M
authors.lastname: Giangiacomi
authors.forename: G
authors.initials: G
authors.lastname: Proietto
authors.forename: C
authors.initials: C
authors.lastname: Feliciani
authors.forename: A
authors.initials: A
authors.lastname: Offidani
authors.forename: G
authors.initials: G
authors.lastname: Bossi
mesh_terms: D000328:Adult; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines / Q000378:metabolism*; D003874:Dermatitis Herpetiformis / Q000378:metabolism*; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D018793:Interleukin-13 / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012867:Skin / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines; D018793:Interleukin-13; D014409:Tumor Necrosis Factor-alpha