The expression of TNF-α and ICAM-1 in lesions of lichen planus and its implication

Abstract

In order to investigate the role of TNF-and ICAM-1 in the pathogenesis of lichen planus, immunohistochemistry was used to detect the expression of TNF-and ICAM-1 in skin lesions of the patients with lichen planus and skin tissues of normal subjects. The results showed that positive rates of TNF-alpha and ICAM-1 expressions in lichen planus were significantly higher than those in normal skins (both P<0.05). Meanwhile, there was a obvious correlation between the increase of TNF-alpha and that of ICAM-1 in lichen planus. The expression of TNF-alpha and ICAM-1 might play an important role in the development of lichen planus.

Association between -308 G/A polymorphism in TNF-α gene and lichen planus: A meta-analysis

“…This may be related to the fact that the functionality of the polymorphism, at least with respect to the extent of the influence on TNF-a level among LP, has not been definitively established. Although potential effect of TNF-a on LP has been described in some studies [10,11], our result implies that the solitary -308 polymorphism may not contribute to LP pathogenesis in a substantial way. When stratified separately according to ethnicity, we found that the A allele carriers (AA + AG) had a significant elevated risk of LP in mixed ethnic population, but not in Caucasians and Asians.…”

“…It was reported to be up-regulated in skin lesions of the patients with LP and oral fluids from OLP patients as compared with controls [10,11]. The expression of TNF-a is regulated at the transcriptional level [12,13], and differences in TNF-a production may partly be determined at the genetic level.…”

Degranulated mast cells and TNF-α in oral lichen planus and oral lichenoid reactions diseases

“…TNF-α is a cytokine that plays the key role in host defense, including immunoregulatory responses implicated in the pathogenesis of many autoimmune and inflammatory diseases[19] such as OLP lesions. TNF-α in this lesions primarily release from degranulated mast cells.…”

Lichen planus

“…The upregulation of the T‐helper‐1 (Th1) arm of cell‐mediated immunity drives basal keratinocyte apoptosis. Implicated cytokines include interferon‐γ, 6 tumor necrosis factor‐α (TNF‐α), 7 additional nuclear factor‐κB (NF‐κB)‐dependent cytokines, such as interleukin‐1α (IL‐1α), IL‐6, and IL‐8, 8 and other apoptosis‐related molecules, such as Fas/Apo‐1 and Bcl‐2 9 . Another mediator may include CXCL10, a chemokine induced by interferon‐γ 10 .…”