Protective cytokine polymorphisms for BA for seven cytokine genotypes (IL-4 -1098/G:T, TNF- alpha -238/G:G, IL-2 -330/G:T, IL-4 -590/C:T, IFNgamma utr5644/A:T, IL-1beta +3962/C:T, IL-10 -1082/A:G), six cytokine diplotypes, four cytokine haplotypes, and four cytokine alleles were found.
The allele and genotype frequencies of a number of polymorphic genes coding for IL-10, TGF-beta, IL-2, IL-12, and IFN-gamma were investigated in 60 patients with asthma in comparison with 140 controls.
Two-gene models implicating functional variants in the IL10 and VDR genes as well as in the IL10 and IL1RL1 genes were associated with asthma (p < 0.0002).
The percentage of CD4(+) CD25(+) Foxp3(+) Treg in the blood and the levels of IL-10 and TGF-beta in the plasma in cases of asthma group were significantly lower than that of the control and therapy group at different time points (P<0.05); The percentage of CD4(+) CD25(+) Foxp3(+) Treg and the level of IL-10 in lymph were significantly higher than that of blood (P<0.05), however, the level of TGF-beta in lymph were significantly lower than that of blood (P<0.05); There were no significant differences which the percentage of CD4(+) CD25(+) Foxp3(+) Treg in the blood and the levels of IL-10 and TGF-beta in the plasma between control group and therapy group (P>0.05).
Reduced airway inflammation in CD26/DPP4-deficient F344 rats is associated with altered recruitment patterns of regulatory T cells and expression of pulmonary surfactant proteins.
To evaluate main effects and gene-gene interactions of haplotype tagging single nucleotide polymorphisms of genes involved in regulatory T-cell function-IL6, IL6R, IL10, heme-oxygenase 1 (HMOX1), IL2, Toll-like receptor 2 (TLR2), TGFB1, TGF-beta receptor (TGFBR)-1, TGFBR2, IL2RA, and forkhead box protein 3 (FOXP3)-in relation to atopy and asthma.
These results suggest that IL-10 plays an important role downstream of the inflammatory cascade in the Th2 response to antigens and in the development of BALF eosinophilia and cytokine production in a murine model of asthma.
To assess the frequency of FLG mutations and the polymorphisms 590 C/T in the IL-4 gene, -1082A/G in the IL-10 gene and -1055C/T in the IL-13 gene in patients with AD and their correlations between severity of AD and asthma.
This review addresses the recent information regarding the association of the polymorphism at position -592 of IL-10 with immune-related diseases including type 2 diabetes with and without nephropathy, multiple sclerosis, and asthma with an emphasize on Iranian patients.
Furthermore, the IL-4Ralpha +1902A/A and IL-1alpha -889C/C homozygous conditions and the TNF-alpha -308G/A, TNF-alpha -238G/A, IL-4 -590T/C and IL-10-1082G/A heterozygous conditions were significantly associated with asthma (p less than 0.05).
We previously identified a steroid-enhancing function of vitamin D in patients with SR asthma in restoring the impaired response to steroids for production of the anti-inflammatory cytokine IL-10.
The levels of MDSCs and IL-10 in asthmatic mice were significantly higher than those in the normal control mice (both p<0.05) and were reduced after budesonide treatment (both p<0.05).
Compared with healthy donors and patients with mild asthma, the percent of CD4+CD25+ Treg cells and plasma IL-10 levels were decreased in patients with moderate to severe asthma.
The asthma susceptibility correlated significantly with IL-10 promoter gene -1082 polymorphism [OR (95 % CI) 1.26 (1.02, 1.55) for AA vs. AG + GG] and -592 polymorphism [OR (95 % CI) 1.12 (1.07, 1.34) for AC + AA vs. CC] (both P < 0.05), but not with -819 polymorphism (P > 0.05).
Additionally, IL-13, IL-10 and eosinophil major basic protein mRNA levels were greater in patients with asthma exacerbations compared to non-exacerbating patients (P = 0.03, P = 0.06 and P = 0.02, respectively), and IL-13 mRNA correlated with the peak Asthma Index (P = 0.006).
Polymorphisms in the identified chitin receptors, NOD2 and TLR9, predispose individuals to inflammatory conditions and dysregulated expression of chitinases and chitinase-like binding proteins, whose activity is essential to generate IL-10-inducing fungal chitin particles in vitro, have also been linked to inflammatory conditions and asthma.
Asthma protection is not conferred by extracts from other enteropathogens and requires a heat-sensitive H. pylori component and the DC-intrinsic production of IL-10.