NF-κB 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-κB.
Skin biopsies of 74 psoriatic cases were studied for the grade of NF-κB staining. They were then correlated with the histopathological indices of severity, especially epidermal hyperplasia and inflammatory infiltrate.
Epidermal nuclear positivity for NF-κB correlated with the grade of epidermal hyperplasia (P = 0.043). There was a significant correlation between grade of basal cell positivity of NF-κB and inflammatory infiltrate (P = 0.004). Lymphocyte staining showed a strong correlation with epidermal and basal cell staining pattern for NF-κB (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-κB to show a positive nuclear stain at the tips of dermal papillae.
The study has demonstrated that translocation of NF-κB 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-κB in lymphocytes, in psoriatic skin leads to NF-κB translocation in the epidermis and basal cells. NF-κB is therefore likely to be one of the key molecules in the pathogenesis of psoriasis.