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Updated: Oct 22, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
Published on: October 12, 2012
Lack of expression of interleukin 8 and RANTES in autoimmune bullous skin diseases
E Bornscheuer1, D Zillikens, J M Schröder
1Department of Dermatology, University of Kiel, Germany.
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.
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