2001
DOI: 10.1046/j.1365-4362.2001.01083.x
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TNFα and IL‐6 are mediators in the blistering process of pemphigus

Abstract: Inflammatory cytokine expression around the blister could play a mediator role in pemphigus lesions by increasing epithelial damage.

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Cited by 86 publications
(66 citation statements)
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“…Our data, using a different approach, such as the basal, mitogen-stimulated proliferation and the DEX mediated inhibition of Con-A stimulated PBMC cytokine secretion in culture medium, reinforce those previous studies. In addition, increased expression of IL-6 and TNF-α around the blistering process of pemphigus has also been reported and could play a mediator role in pemphigus lesions by increasing epithelial damage [44]. More recently, the presence of TNF-α, IFN-γ, and IL-1 in the inflammatory exudates of lesions and an expression of proinflammatory cytokines, such as TNF-α and IL-6, around the blister were demonstrated in pemphigus patients by in situ hybridization.…”
Section: Discussionmentioning
confidence: 98%
“…Our data, using a different approach, such as the basal, mitogen-stimulated proliferation and the DEX mediated inhibition of Con-A stimulated PBMC cytokine secretion in culture medium, reinforce those previous studies. In addition, increased expression of IL-6 and TNF-α around the blistering process of pemphigus has also been reported and could play a mediator role in pemphigus lesions by increasing epithelial damage [44]. More recently, the presence of TNF-α, IFN-γ, and IL-1 in the inflammatory exudates of lesions and an expression of proinflammatory cytokines, such as TNF-α and IL-6, around the blister were demonstrated in pemphigus patients by in situ hybridization.…”
Section: Discussionmentioning
confidence: 98%
“…Pemphigus is a disease of middle age , in the present study 3 out of 6 patients are in age group 41-50 years. According to Lopez-Robles E etal [5] , almost all pemphigus vulgaris have oral involvement. In present study 5 patients diagnosed as pemphigus vulgaris, 80% has oral involvement.…”
Section: Discussionmentioning
confidence: 99%
“…Most probably, microorganisms could trigger TLR3/ TLR4, which expression is increased in KCs of PF patients leading to NF-kB activation [37]. The activation of TLR pathways leads to proinflammatory cytokine secretion, which could maintain the chronic activation of the CD4+ T-cell in PF [38,39]. Thus, after stimulation by bacterial products, TLRs mediate a variety of signals not only for inducing pro-inflammatory cytokines, such as TNF-α, IL-6, INF-γ, and IL-12, but also for up-regulated co-stimulatory molecules, such as CD80 and CD86 to activate immune responses [40].…”
Section: Discussionmentioning
confidence: 99%