Role of NF-κB in the pathogenesis of psoriasis elucidated by its staining in skin biopsy specimens

Background NF-B is a transcription factor belonging to the Re1 family, and it regulates the activity of a large number of proinflammatory genes. Its role in psoriasis, which is a prototype chronic inflammatory disease, is therefore expected to be considerable. It has been found that many of the triggering factors for psoriasis initiate inflammation by activation of NF-B. Methods Skin biopsies of 74 psoriatic cases were studied for the grade of NF-B staining. They were then correlated with the histopathological indices of severity, especially epidermal hyperplasia and inflammatory infiltrate. Results Epidermal nuclear positivity for NF-B correlated with the grade of epidermal hyperplasia (P=0.043). There was a significant correlation between grade of basal cell positivity of NF-B and inflammatory infiltrate (P=0.004). Lymphocyte staining showed a strong correlation with epidermal and basal cell staining pattern for NF-B (P=0.004 and 0.003, respectively). There was, however, no correlation of lymphocyte staining with any histopathological parameter. There was also a peculiar propensity for NF-B to show a positive nuclear stain at the tips of dermal papillae. Conclusions The study has demonstrated that translocation of NF-B in the epidermis and basal cells is responsible for two of the key pathological features of psoriasis, epidermal hyperplasia, and inflammation. We have postulated that translocation of NF-B in lymphocytes, in psoriatic skin leads to NF-B translocation in the epidermis and basal cells. NF-B is therefore likely to be one of the key molecules in the pathogenesis of psoriasis.