To investigate TLR2 and TLR4 expression on PB monocytes during AD exacerbation and to assess the relationships between TLR expressions with AD clinical severity and with serum interleukin (IL) 4, IL-10, and IL-17a levels.
Interestingly, IL-10 mRNA expression by purified T cells of children with allergic and non-allergic asthma and children with atopic dermatitis was strongly decreased as compared with that of healthy controls.
FLG mutation, alone and in combination with certain IL-10 or IL-13 polymorphisms, enhances the risk for the development of AD in the Polish population.
The current evidence does not support a strong genetic relationship between IL-10-1082 A/G, - 819 T/C and - 592 A/C polymorphisms and the susceptibility to atopic dermatitis.
Our results demonstrate for the first time that IL-10 receptors may have a role in the pathogenesis of atopic eczema and its upregulation by FK506 and UVA could explain the therapeutic efficacy of these agents.
The results showed promoting effects of auraptene on T cell subsets toward Th<sub>1</sub> (IFN-γ) and T<sub>reg</sub> (IL-10), which suggest its therapeutic value for treatment of Th<sub>2</sub> cells predominant diseases including allergic disease such as asthma and atopic dermatitis as well as cancers.
The allele and genotype frequencies of genes encoding for IL-10 and TGF-β1 were investigated in 89 patients with atopic dermatitis in comparison with 138 in the control group using the PCR-SSP method.
Protective cytokine polymorphisms for AD for seven cytokine genotypes (IL-4 -1098/G:T, TGFbeta cdn25/G:G, IL-4 -33/C:C, IL-1alpha -889/C:C, IFNgamma +874/A:A, IL-10 -1082/A:A, IL-1beta -511/C:C), one cytokine diplotypes, two cytokine haplotypes, and four cytokine alleles were also found.
Using amplification refractory mutation screening PCR, we examined TGFB1 and IL10 gene polymorphisms, which are known to affect cytokine production, in 68 children with moderately severe AD and in 50 nonatopic children.
We also investigated the inhibitory capacity of WIKIM30 on the development of 2,4-dinitrochlorobenzene-induced atopic dermatitis (AD), a Th2-dominant allergic disease in mice.Oral administration of <i>L. sakei</i> WIKIM30 significantly reduced AD-like skin lesions and serum immunoglobulin E and IL-4 levels while decreasing the number of CD4<sup>+</sup> T cells and B cells and the levels of Th2 cytokines (IL-4, IL-5, and IL-13) in peripheral lymph nodes and enhancing Treg differentiation and IL-10 secretion in mesenteric lymph nodes.
SNPs at positions -3575, -2849, -2779, -2763, -1082, -851, -819 and -592 in the IL10 promoter region were genotyped in individuals with atopic dermatitis (n= 47) and nonatopic control subjects (n= 40) using polymerase chain reaction-based techniques and induced heteroduplex generator (IHG) analysis.
This study examined the expression of the immunosuppressive cytokines TGF-beta and IL-10, the Th2-type cytokines IL-4 and IL-6, and the Th1-type cytokines IFN-gamma, TNF-alpha, IL-2, IL-12p35 and IL-12p40, in canine atopic dermatitis.
Our findings indicate a potential role of IDEC-like in the maintenance of inflammation in atopic dermatitis patients; moreover, IDEC-like may exert a regulatory impact on T cells of AD individuals through IL-10, often induced by agonist mimicking single stranded RNA virus.
In our study, genotypes of 7 polymorphisms--LL-4 -1098G/T and -590C/T, IL-6 -174C/G and nt565A/G, and IL-10-1082A/G, -819C/T, and -592A/C were significantly associated with atopic AD (P < .05).
The increased level of SP, in atopic dermatitis, induces the release of interferon (IFN)-γ, interleukin (IL)-4, tumor necrosis factor (TNF)-α, and IL-10 from the peripheral blood mononuclear leukocytes.
After adjusting for multiple tests, the association between IL13 130 and IgE and the interactive effects of IL10-1082 on current rhinitis and IL8 781 on atopic eczema were significant by controlling a false-positive rate of 0.05 and 0.10, respectively.
Having a dog in infancy is associated with higher IL-10 and IL-13 cytokine secretion profiles and reduced allergic sensitization and atopic dermatitis.