The combination of QIV and LGG reduced inflammatory responses (i.e., IFN-γ, IL17A, IL-17F, IL-6, and TNF-α) from activated PBMCs of pediatric patients with T1D, without dampening the production of seroprotective antibodies.
Interestingly, treatment with IL-6 and TNF-α inhibitors in primary hNPCs and hAFCs that were isolated from patients with IDD led to the downregulation of CUL4A and CUL4B.
Our findings suggest that LTA rs909253 and TNFrs1800629 polymorphisms are associated with the risk of T1D both independently and in combination with polymorphic markers in other inflammatory genes, and the analysis of multi-allelic combinations provides valuable insight in the study of polygenic traits.
In conclusion, this study indicated that aerobic exercise training by a decrease of HbA1c and plasma IL-6, TNF-α and IL-1β could decrease MSTN levels in plasma and skeletal muscle in T1DM.
Five studies in 3316 subjects assessed TNFRs with renal disease in patients with type 1 diabetes and showed both TNFR-1 and TNFR-2 were consistently associated with the renal outcomes.
In addition, the blood chemistry profile complements the TEM data as demonstrated by an increase in serum levels of alanine aminotransferase (ALT), dyslipidemia, C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and malondialdehyde (MDA) by T1DM that were significantly (p < 0.05) reduced with insulin injections.
Our data concluded that IFN-γ +874T allele, TNF-α -308A allele, IL-1β -511T allele, and IL-4 -590T allele could be considered risk factors for T1D development in Saudi subjects.
Meta-analysis to collect all the relevant studies to further investigate whether or not the FAS ligand (FASL) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) genetic polymorphisms are associated with susceptibility to intervertebral disc degeneration (IDD) in Chinese Han population.
MIN6 and EndoC-βH1 beta cell lines and human islets were treated with IL-1β, IFN-γ and TNF-α to mimic the inflammatory milieu of early type 1 diabetes.
Proinflammatory cytokines such as IL-1<i>β</i>, IL-6, TNF-<i>α</i>, IFN-<i>γ</i>, IL-12, IL-17, and NO can be released by CD4 and CD8<sup>+</sup> lymphocytes as well as by classically activated macrophages (CAM<i>ϕ</i>s), which are important in the development of T1D.
Studies have investigated the correlation between tumor necrosis factor related apoptosis-inducing ligand (TRAIL) gene polymorphisms and the susceptibility and severity of intervertebral disc degeneration (IDD), but the results were inconsistent.
Fibroblasts from T1D subjects accumulated more lipid, had higher LC-CoA levels and converted more FA to CO2, with less mitochondrial proton leak in response to oleate alone or with TNFα, using the latter as a model of inflammation.
Proinflammatory cytokines including interleukins, interferons, transforming growth factor-β, tumor necrosis factor-α, and nitric oxide promote destructive insulitis in type 1 diabetes through amplification of the autoimmune reaction, direct toxicity to β-cells, and sensitization of islets to apoptosis.
The expression of Pdx1, NF-κb, IKB genes in the pancreas and plasma TNF-α levels in T1- and T2DM; Nrf2, Glut2, COX2, and iNOS proteins in pancreatic tissue of T1DM and LPCLN2, NF-κb, IKB I in adipose tissue of T2DM reverted to normal in LXA4-treated animals.
Bone expression analyses revealed that tumor necrosis factor (TNF)-α levels were highest in T1D-OVX mice and correlated with bone loss, and osteoblast and osteocyte death.
The objective of this study was to determine the effect of TNF-α expression of osteocytic RANKL and sclerostin in type 1 diabetes rats with periodontitis using infliximab (IFX), a TNF-α antagonist.