Moorchung Nikhil, Vasudevan Biju, Mani N S, Verma Rajesh
Department of Pathology, Armed Forces Medical College, Pune, Maharashtra, India.
Indian J Pathol Microbiol. 2014 Apr-Jun;57(2):205-8. doi: 10.4103/0377-4929.134664.
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.
肿瘤坏死因子-α(TNF-α)是银屑病发病机制中的重要介质。核因子-κB(NF-κB)是一种调节促炎基因活性的转录因子。银屑病是一种炎症性疾病,TNF-α和NF-κB的作用值得关注。
我们研究了TNF-α和NF-κB在银屑病中的作用。
共研究了61例银屑病皮肤活检病例,TNF-α和NF-κB的染色分级与严重程度的组织病理学指标相关。
Pearson相关系数和卡方检验。使用社会科学统计软件包第13版。
表皮细胞和基底细胞胞质中的TNF-α免疫染色与表皮增生分级呈强烈负相关(分别为P = -0.019和P = -0.009)。表皮细胞胞质中TNF-α的阳性和淋巴细胞阳性与表皮细胞核、基底细胞或淋巴细胞中NF-κB免疫染色分级无关。基底细胞胞质中TNF-α的阳性与基底细胞核中NF-κB免疫染色分级在P = 0.005时有相关性。表皮胞质中TNF-α免疫染色与淋巴细胞免疫染色之间有强烈相关性(P = -0.08);然而,其他两个部位的TNF-α表达之间无相关性。
本研究概述了NF-κB与TNF-α之间的关系及其在银屑病特征性组织病理学变化发展中的联合作用。我们假设NF-κB参与刺激TNF-α的释放,这可以解释银屑病的特征性组织病理学变化。然而,在银屑病发病机制中,NF-κB也可能独立于TNF-α发挥作用。