As the NK cell receptor KIR2DL4 has been reported to induce interferon gamma (IFNγ) secretion when ligated with HLA-G, we postulated that the 9A/10A genetic polymorphism of KIR2DL4 which influences receptor structure may influence susceptibility to asthma.
C. pneumoniae-induced IFN-γ production in vitro was more prevalent in asthma compared with non-asthma; levels of IFN-γ were higher in asthma compared with non-asthma (P = 0.003).
The characterization of CCR10<sup>+</sup> ILC2s in human samples and in mouse asthma models suggests that these cells downregulate allergic inflammation through IFN-γ production.
Using these approaches, studies have suggested that genes within the cytokine gene cluster on chromosome 5 (including interleukins-3, -4, -5, -9, and -13), chromosome 11 (the beta chain of the high affinity IgE receptor), chromosome 16 (the IL-4 receptor), and chromosome 12 (stem cell factor, interferon-gamma, insulin growth factor, and Stat 6 [IL-4 Stat]) may contribute to asthma and allergy development.
We selected the IFNG locus on 12q21 as a candidate gene for asthma on the basis of its role in pathophysiology and positive linkage demonstrated in other populations.
The median BALF concentrations of IL-33, TSLP, IL-4, IL-5, IL-13, and IL-12p70, but not IL-25, IL-2, or IFN-γ, were significantly elevated in asthmatics compared with controls (<i>p</i> < 0.05).
The levels of IgE, EO and IL-4 in the children with asthma were obviously higher than those in normal controls, while the level of IFN-γ in patients with asthma was significantly lower than that in healthy subjects.
The significant increase of asthma incubation period, serum IFN-γ level were observed in the asthma guinea pigs treated with the active components group.
IFN-γ expression was lower among patients with the AA genotype than those with the AT genotype (P<0.05); the genotypic and allelic frequency distributions of the IL-4 gene at -33C/T and -589C/T were significantly different between the asthmatic children and the control (P<0.05).
After correction for multiple comparisons, 7 SNPs in 6 genes (CARD25, TGFB1, LY96, ACAA1, DEFB1, and IFNG) were associated with asthma (adjusted p-value<0.02), while 5 SNPs in 3 different genes (CD80, STAT4, and IRAKI) were significantly associated with eczema (adjusted p-value < 0.02).
In a previous analysis of 372 children from the Boston Home Allergens and the Connecticut Childhood Asthma studies, 7 SNPs in 6 genes (CARD15, TGFB1, LY96, ACAA1, DEFB1 and IFNG) involved in innate immune pathways were associated with asthma, and 5 SNPs in 3 genes (CD80, STAT4, IRAK2) were associated with eczema.
In comparison with that in the healthy control (HC), significantly lower abundance of Bifidobacterium and lower levels of Th1 cytokines (IFN-γ and TNF-α), but higher levels of Th2-type cytokines (IL-4, IL-5) and Th17-type (IL-17A) cytokine were detected in children with bronchiolitis and asthma.
This study investigated CA repeats polymorphism of the IFN-gamma gene and GT repeats polymorphism of the IRF-1 gene, which may predispose individuals to asthma pathogenesis.
In CD4+ T cells treated with PMA+MLIF, the expression levels of IFN-γ, TNF-α and IL-4 were strongly inhibited (p<0.001, p<0.001 and p<0.0094), compared to PMA treatment alone, for both, rhinitis and asthma.
Effects of Astragalus membranaceus in promoting T-helper cell type 1 polarization and interferon-gamma production by up-regulating T-bet expression in patients with asthma.
Prednisolone treatment in asthma. Reduction in the numbers of eosinophils, T cells, tryptase-only positive mast cells, and modulation of IL-4, IL-5, and interferon-gamma cytokine gene expression within the bronchial mucosa.
In conclusions, through the modification of the expression of CCR-3 in peripheral blood leukocytes from atopic asthmatics, IFN-gamma could exert a beneficial effect in patients with asthma, regulating the migration of some inflammatory cells involved in the pathogenesis of the disease.
The findings showed that the extract of <i>Z. multiflora</i> decreased pro-inflammatory cytokines in asthma (IL-4 and IL-17 and TGF-β) but increased anti-inflammatory cytokines (IFN-γ) gene expression and the number of Treg (FOXP3) in splenocytes of asthmatic mice which may indicate the specific therapeutic effect of the plant extract in allergy, autoimmunity, and infectious diseases via potentiating Th<sub>1</sub> and suppressing Th2 and Th<sub>17</sub> cells.