Evaluation of survivin and NF-kappaB in psoriasis, an immunohistochemical study

Suppression of apoptosis is generally one of the accepted pathogenetic mechanisms for psoriasis and any epidermal hyperproliferative states. Survivin is a member of the inhibitor of apoptosis protein family mediating its apoptosis suppressive function by the inhibition of caspase pathway. Nuclear factor kappa B (NF-kappaB) is a transcription factor that regulates hundreds of genes including many critically involved in apoptosis. The aim of this study was to explore the role could be played by survivin and NF-kappaB in psoriasis and the link between them.

Thirty cases of lesional psoriasis, 10 perilesional and 10 control specimens from normal skin were studied by immunohistochemical method for expression of survivin and NF-kappaB.

Survivin was detected in 73% of psoriatic lesions distributed either in epidermis, in endothelial cells of proliferating capillaries or in both of them. In non-psoriatic lesions either perilesional or control specimens, survivin was confined to basal layer of epidermis, significantly up regulated in psoriasis in comparison with non-psoriatic lesions (p = 0.0001). Nuclear expression of NF-kappaB was detected in 66% of psoriatic lesions; this active phosphorylated form was significantly over expressed in psoriasis in comparison with normal skin (p = 0.0004). Diffuse nuclear expression of NF-kappaB was significantly associated with up-regulation of survivin in psoriatic plaque (p = 0.03).

Survivin and NF-kappaB appeared to be important factors in the pathogenesis of psoriasis. Survivin could be the target of NF-kappaB mediating its death signal inhibition pathway in psoriasis.