Expression of eotaxin, interleukin 13 and tumour necrosisfactor-alpha in dermatitis herpetiformis

Citation
P. Amerio et al., Expression of eotaxin, interleukin 13 and tumour necrosisfactor-alpha in dermatitis herpetiformis, BR J DERM, 143(5), 2000, pp. 974-978
Citations number
33
Categorie Soggetti
Dermatology,"da verificare
Journal title
BRITISH JOURNAL OF DERMATOLOGY
ISSN journal
00070963 → ACNP
Volume
143
Issue
5
Year of publication
2000
Pages
974 - 978
Database
ISI
SICI code
0007-0963(200011)143:5<974:EOEI1A>2.0.ZU;2-R
Abstract
Background The dermal and perivascular infiltrate in dermatitis herpetiform is (DH), which is mainly composed of CD4+ lymphocytes, neutrophils and eosi nophils, is believed to play an important part in the pathogenesis of the d isease. 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 eota xin, which is a highly specific chemotactic protein induced by various cyto kines [IL-4, IL-13, tumour necrosis factor (TNF)-alpha and interferon-gamma ]. Objectives To evaluate the expression of eotaxin and its inducers, IL-13 an d TNF-alpha, in DH. Methods We examined lesions collected from 10 DH patients with active disea se. Sections from each specimen were incubated with anti-IL-13, anti-TNF-al pha and anti-eotaxin antibodies. Chloroacetyl esterase reaction was perform ed to show mast cell infiltration. Results Eotaxin was mainly expressed at the tips of the dermal papillae, wi thin the microabscesses. Positivity was also found in the lymphomonocytic i nfiltrate in the dermis. IL-13 was expressed in the dermal infiltrate and T NF-alpha was found in the inflammatory infiltrate and in dermal vascular ce lls. Conclusions These findings confirm the importance of the lymphomonocytic in filtrate and of Th2 cytokines in the pathogenesis of this disease, suggesti ng that tissue infiltration in DH is mediated by cell-specific chemokines s uch as eotaxin and not only by non-specific chemokines such as IL-8.