TNFα and IL‐6 are mediators in the blistering process of pemphigus

Lopez-Robles, Erendira; Avalos‐Díaz, Esperanza; Vega‐Memije, Elisa; Hojyo‐Tomoka, Teresa; Villalobos, R.; Fraire, Saúl; Domíguez‐Soto, Luciano; Herrera‐Esparza, Rafael

doi:10.1046/j.1365-4362.2001.01083.x

Cited by 85 publications

(66 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…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%

Glucocorticoid Sensitivity and Proinflammatory Cytokines Pattern in Pemphigus

2012

View full text Add to dashboard Cite

Glucocorticoids (GC) represent the main treatment for pemphigus; however, some patients show GC resistance. GC sensitivity was evaluated in 19 pemphigus patients and 41 controls by the number of binding sites [B max (fmol/mg protein)] and the affinity of GC receptor [Kd (nM)] to dexamethasone (DEX) as well as by the pattern of cytokine by DEXmediated inhibition of concanavalin-A (Con-A)-stimulated PBMC proliferation. The Kd (15.7±2.8 vs.8.1±1.3) and Bmax (6.5±0.9 vs. 3.9±0.3) were higher in pemphigus than controls (p00.002). Considering the values above the 95th percentile of normal group as a cut-off (K d >24.9 nM and B max >8.1 fmol/mg protein), elevated K d and B max were observed in 9.8% and 2.4% of controls and 15.8% and 36.8% of patients (p00.02). PBMC proliferation was stimulated by Con-A and inhibited by DEX (p<0.001) in both pemphigus and control groups. IL-6 and TNFα (pg/mL) basal production were higher in patients than controls. There was an increment of these cytokines after Con-A stimulation, and they were inhibited by DEX (p00.002) in controls and remained elevated in pemphigus (p<0.02). Patients and controls showed no difference in basal and stimulated production of IL-8 and IL-10. There is an alteration on GC sensitivity in pemphigus patients and a higher production of proinflammatory cytokines. Therefore, in pemphigus patients, proinflammatory cytokines might be involved in the mechanism of GC resistance and/or in its maintenance.

show abstract

Section: Discussionmentioning

confidence: 98%

Glucocorticoid Sensitivity and Proinflammatory Cytokines Pattern in Pemphigus

2012

View full text Add to dashboard Cite

show abstract

“…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%

Clinical, Histological and Direct Immunofluorescence Study in Immunobullous Diseases

Nageswaramma¹,

Naik²,

Rao³

2016

IOSR

View full text Add to dashboard Cite

“…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%

Potential Role of TLR Ligand in Aethiopathogenesis of Tunisian Endemic Pemphigus Foliaceus

D¹

2013

Biochem Physiol

View full text Add to dashboard Cite

Pemphigus foliaceus (PF) is an autoimmune skin disease in which environmental factors are thought to participate. Recent studies suggest that microbial components use signaling molecules of the human Toll-like receptor (TLR) family to transduce signals in keratinocytes. The aim of our research was to investigate the expression of TLRs 2, 3 and 4 by keratinocytes of PF patients compared to normal keratinocytes, in order to characterise the nature of the microbial factor involved in the etiopathology of PF. Biopsies obtained from 43 PF patients and 20 healthy controls were assessed by immunohistochemical analysis using specific polyclonal antibodies. The TLR2, TLR3 and TLR4 expression was significantly upregulated in PF epidermis. The significant increase of those TLRs simultaneously may merely reflect the complicated environmental conditions of rural women in the southern rural regions of Tunisia. Interestingly, we have found that the TLR4 diffuse expression was associated with the production of anti-desmoglein 1 Abs (p=0.037). This could be in line with a potential role of TLR ligand in aethiopathogenesis of Tunisian endemic PF.TLR over-expression in pemphigus skin indicates that TLRs are involved in the pathogenesis of pemphigus through stimulation by infectious or endogenous ligands.

show abstract

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.

Cited by 85 publications

References 19 publications

Glucocorticoid Sensitivity and Proinflammatory Cytokines Pattern in Pemphigus

Glucocorticoid Sensitivity and Proinflammatory Cytokines Pattern in Pemphigus

Clinical, Histological and Direct Immunofluorescence Study in Immunobullous Diseases

Potential Role of TLR Ligand in Aethiopathogenesis of Tunisian Endemic Pemphigus Foliaceus

Contact Info

Product

Resources

About