Does epstein-Barr virus-encoded EBNA1 inhibit the canonical NF-kappaB pathway in carcinoma cells by inhibiting IKK phosphorylation?
Inhibition of p65 NF-kappaB in murine and human epidermis results in tissue hyperplasia and the development of squamous cell carcinoma. In line with this, p65 knockout fibroblasts have a transformed phenotype. Inhibition of p65 NF-kappaB by EBNA1 may therefore contribute to the development of NPC by inducing tissue hyperplasia. Furthermore, inhibition of NF-kappaB is employed by viruses as an immune evasion strategy which is also closely linked to oncogenesis during persistent viral infection. Our findings therefore further implicate EBNA1 in playing an important role in the pathogenesis of NPC.
The exposure of CD4+ and CD8+ cells on allergen may induce the Fas-FasL apoptotic pathway. Significant decrease in number of allergen-reactive CD4+, CD8+ cells after SIT suggests participation of the phenomenon in deletion of clones, which may be a part of the allergen tolerance mechanism achieved naturally or during SIT.