Comparison of expression of heat‐shock protein 60, Toll‐like receptors 2 and 4, and T‐cell receptor γδ in plaque and guttate psoriasis

Abstract

Psoriasis is a chronic skin disease that appears to be autoimmune in nature. Recently, it is thought that microbial pathogens of skin can affect the pathogenesis of psoriasis by inducing autoimmunity. Heat-shock proteins (HSPs) are known to play an important role in immune and inflammatory responses of the skin including psoriasis. Recent studies have suggested that Toll-like receptors (TLR) 2, 4 and gammadelta T-cell receptors (TCR-gammadelta) may recognize HSP60 as a ligand and consequently activate the immune system. The biopsy specimens of 12 of guttate psoriasis, 12 of plaque psoriasis and five of normal skin were studied using immunohistochemical staining. The expressions of HSP60, TLR2 and TLR4 were evaluated using an immunostaining-intensity-distribution (IID) index and TCR-gammadelta positive cells were counted. The expression of HSP60 was significantly higher in guttate and plaque psoriasis than in normal skin. The expression of TLR4 was higher in guttate psoriasis than in plaque psoriasis and normal skin. The expression of TCR-gammadelta was higher in guttate and plaque psoriasis than in normal skin, but there was no correlation found between the expression of HSP60 and TLRs 2 and 4, or between that of HSP60 and TCR-gammadelta. HSP60 may be related to the pathogenesis of both guttate and plaque psoriasis and TLR4 may be related to the pathogenesis of guttate psoriasis.