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.


CONCLUSIONS
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.
D001327:Autoimmune Diseases / Q000378:metabolism*; D001768:Blister / Q000378:metabolism; D018946:Chemokine CCL5 / Q000378:metabolism*; D003874:Dermatitis Herpetiformis / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D007070:Immunoglobulin A / Q000032:analysis; D007150:Immunohistochemistry; D016209:Interleukin-8 / Q000378:metabolism*; D010391:Pemphigoid, Bullous / Q000378:metabolism; D010392:Pemphigus / Q000378:metabolism; D012867:Skin / Q000378:metabolism; D012872:Skin Diseases, Vesiculobullous / Q000378:metabolism*