Abstract
The question of the effect of anti-TNF-alpha in skin carcinogenesis is especially relevant in view of the increased use of these drugs for the treatment of autoinflammatory immune diseases. Since ultraviolet radiation and human papillomavirus are involved in skin carcinogenesis, we wished to investigate the effect of TNF-alpha antagonists on the UVB-induced apoptosis of keratinocytes infected by HPV38. Our results indicate that anti-TNF agent, infliximab, does not contribute to the survival of HPV38-transduced keratinocytes with UVB-induced DNA damages.
Highlights
Tumor necrosis factor-alpha (TNF-α) is one of the main mediators of skin and mucosa inflammation and has a potent antiproliferative effect on normal epithelial cells
Exposure to exogenous TNFα resulted in a significant increase of UVB-induced apoptosis with no significant difference in both pLXSN-HaCaT and HPV38 E6/E7-HaCaT cells
Our results confirm recent data [11] demonstrating that HPV38 E6 and E7 expression in human primary keratinocytes was associated with a low level of UVB-induced apoptosis through the expression of NF-κB- regulated survival factor genes favoring the survival of keratinocytes
Summary
Tumor necrosis factor-alpha (TNF-α) is one of the main mediators of skin and mucosa inflammation and has a potent antiproliferative effect on normal epithelial cells. Several epidemiological studies have reported an increased risk of nonmelanoma skin cancer in patients treated with anti-TNF agents, the relationship remains uncertain [2]. The question of the effect of anti-TNF-α in skin carcinogenesis is, especially relevant in view of the increased use of these drugs for the treatment of autoinflammatory immune diseases. Besides ultraviolet (UV) irradiation which is the most important risk factor involved in the development of NMSC, cutaneous beta-HPV infection is considered as an important cofactor [3]. There are no available data on the interactions between cutaneous HPV infection and anti-TNF agents
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