Vitiligo
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Therefore, we investigated the TNF-alpha-308 SNP in patients with vitiligo.We examined 61 patients with vitiligo.
|
16691430 |
2006 |
Vitiligo
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Since the presence of A nucleotide at position -308 of TNF-alpha gene is associated with increased cytokine production, therefore, the higher frequency of TNF-alpha -308 A allele in vitiligo patients compared to controls may be considered as a genetic susceptibility factor towards the development of vitiligo.
|
18820938 |
2009 |
Vitiligo
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The study's findings demonstrate that the studied hypopigmented (vitiligo, hypopigmented MF, hypopigmented TV) disorders show similar changes in their cutaneous microenvironment with increased TNF-α and decreased bFGF mRNA expression.
|
22151832 |
2013 |
Vitiligo
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In particular, haplotypes: AATCC, AACCT, AGTCT, GATCT, GATCC and AGCCT were found to increase the TNF-α levels in vitiligo patients.
|
23284977 |
2012 |
Vitiligo
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The frequency of allele A (TNF-α 2-allele) was significantly higher and that of allele G (TNF-α 1-allele) was lower in vitiligo patients compared to controls, indicating an association of allele A with susceptibility to vitiligo in Saudi patients.
|
23884763 |
2013 |
Vitiligo
|
0.400 |
Biomarker
|
disease |
BEFREE |
TNFα emerges as a complex mediator with apparently conflicting roles in vitiligo.
|
23912226 |
2013 |
Vitiligo
|
0.400 |
Biomarker
|
disease |
BEFREE |
We have earlier reported the role of TNFA in autoimmune pathogenesis of vitiligo, and we now show the involvement of TNFB in vitiligo pathogenesis.
|
24312346 |
2013 |
Vitiligo
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Serum IL-10 and TNF-α levels were higher in the vitiligo group (P = 0.001).
|
25283497 |
2015 |
Vitiligo
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
We investigated whether the tumor necrosis factor-a (TNF-α) promoter -238 A/G and -308 A/G polymorphisms are associated with rheumatoid arthritis (RA) and vitiligo susceptibility.
|
26125752 |
2015 |
Vitiligo
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Data for a total of 1505 vitiligo cases and 2253 controls from five case-control studies concentrating on the association between TNF-α-308 G/A polymorphism and vitiligo were included in this meta-analysis.
|
26224639 |
2015 |
Vitiligo
|
0.400 |
Biomarker
|
disease |
BEFREE |
We also investigated AHR-related cytokines and observed increased serum TNF-α concentration and diminished serum levels of IL-10 and TGF-β1 in vitiligo.
|
26370050 |
2015 |
Vitiligo
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Studies reporting the association between TNF-α-308G/A polymorphism and vitiligo risk were retrieved from PubMed and EmBase databases.
|
26681224 |
2015 |
Vitiligo
|
0.400 |
Biomarker
|
disease |
BEFREE |
Our aim was to investigate the role of IFN-γ expression and polymorphism in vitiligo susceptibility and whether intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor (TNF)-α, and TNF-β play a role in vitiligo pathogenesis as important inflammatory parameters.
|
28273427 |
2017 |
Vitiligo
|
0.400 |
Biomarker
|
disease |
CTD_human |
Depigmented epidermis of vitiligo patients also showed lower levels of Nrf2 and phospho-PI3K but higher levels of ROS, TNF-ɑ, IL-1ɑ, and ROS with more TUNEL-positive cells.
|
28836394 |
2017 |
Vitiligo
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Serum IL-2, -6, -17, -22, and TNF-α levels were measured by enzyme-linked immunosorbent assay (ELISA) in all patients and healthy controls, and their levels were correlated with the extent, duration, and activity of vitiligo.
|
29504235 |
2019 |
Vitiligo
|
0.400 |
Biomarker
|
disease |
BEFREE |
The expression levels of IL-6, IL-17 and TNF-α in patients with progressive vitiligo were significantly higher than those in patients with stable vitiligo (P<0.05).
|
30651813 |
2019 |
Vitiligo
|
0.400 |
Biomarker
|
disease |
BEFREE |
Additionally, enrichment analysis suggested that targets of KBL on vitiligo were mainly clustered into multiple biological processes (associated with DNA translation, lymphocyte differentiation and activation, steroid biosynthesis, autoimmune and systemic inflammatory reaction, neuron apoptosis, and vitamin deficiency) and related pathways (TNF, JAK-STAT, ILs, TLRs, prolactin, and NF-<i>κ</i>B), indicating the underlying mechanisms of KBL on vitiligo.
|
31781265 |
2019 |