Expression of tumor necrosis factor-α and nuclear factor-kappaB/RelA and the pathogenesis of psoriasis

Tumor necrosis factor-α (TNF-α) is an important mediator in the pathogenesis of psoriasis. Nuclear factor-kappaB (NF-κB) is a transcription factor that regulates the activity of the proinflammatory genes. Psoriasis is an inflammatory disease and the role of TNF-α and NF-κB, should be considerable. We studied the role of TNF-α and NF-κB in psoriasis. A total of 61 cases of psoriatic skin biopsies were studies and the grade of TNF-α and NF-κB, staining was correlated with the histopathological indices of severity. Pearson's correlation coefficient and Chi-square test. Statistical Package for Social Sciences version 13 was used. The TNF-α immunostain in the cytoplasm of the epidermal cells and basal cells showed a strong inverse correlation with the grade of epidermal hyperplasia (P -0.019 and P -0.009, respectively). The epidermal cytoplasmic positivity and lymphocyte positivity for TNF-α did not correlate with the grade of NF-κB immunostaining in the epidermal cell nuclei, basal cells or lymphocytes. The basal cell cytoplasmic positivity for TNF-α correlated with the grade of NF-κB immunostaining in the nucleus of basal cells at a P - 0.005. There was a strong correlation between the epidermal cytoplasmic TNF-α immunostaining with the lymphocyte immunostaining (P -0.08); however, there was no correlation between the TNF-α expression in the other two locations. The study outlines the relationship between NF-κB and TNF-α and their combined role in the development of the characteristic histopathological changes in psoriasis. We hypothesize that NF-κB is involved in stimulating the release of TNF-α which would account for the characteristic histopathological changes of psoriasis. However, it is likely that NF-κB can act independently of TNF-α also in the pathogenesis of psoriasis.