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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Lack of expression of interleukin 8 and RANTES in autoimmune bullous skin diseases.

BACKGROUND: In autoimmune bullous skin diseases, accumulation of neutrophils and/or eosinophils in the affected skin represents a characteristic feature. So far, however, the induction of this granulocyte infiltration has not been elucidated. OBJECTIVE: Regarding their biological effects, the chemokines interleukin 8 (IL-8) and RANTES (regulated upon activation normal T lymphocyte expressed and secreted) could play a role in this granulocyte accumulation. METHODS: Immunohistochemical examination of lesional skin from patients with bullous pemphigoid, pemphigus, dermatitis herpetiformis and linear IgA disease was performed using a set of different antibodies against IL-8 and RANTES. Additionally, blister fluids were screened for soluble RANTES peptide using an ELISA. RESULTS: No difference in chemokine expression was found in lesions of autoimmune bullous diseases compared to normal skin. CONCLUSION: In contrast to chronic inflammatory diseases like psoriasis and eczema, where keratinocyte IL-8 immunoreactivity was found to differ from normal skin, keratinocyte immunoreactivity is not altered in autoimmune bullous diseases.[1]


  1. Lack of expression of interleukin 8 and RANTES in autoimmune bullous skin diseases. Bornscheuer, E., Zillikens, D., Schröder, J.M., Sticherling, M. Dermatology (Basel) (1999) [Pubmed]
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