IL-1 receptor–type expression in relation to atopy

Soluble Interleukin‐1 Receptor Type II Levels in Gingival Crevicular Fluid in Aggressive and Chronic Periodontitis

“…IL‐1RII protects against inflammatory disease by acting as a decoy receptor and regulates IL‐1 activity 12 . Gupta and Bewtra 19 compared the concentrations of sIL‐1RI and −1RII and IL‐1β in sera and supernatants of cultured peripheral blood mononuclear cells from atopic and non‐atopic subjects; the levels of both soluble receptors from the serum and supernatant of non‐atopic donors were higher than those in atopic donors. Although the level of sIL‐1RI did not correlate with indices of disease activity (Larsen score) or joint destruction, sIL‐1RII serum levels in patients with non‐destructive arthritis were higher than those in patients with destructive arthritis 20 .…”

“…Inhibition of IL‐1RII mRNA production by IFN‐γ correlated with the decreased production of sIL‐1RII protein, which demonstrates that decreased IL‐1RII gene expression results in reduced IL‐1RII protein synthesis 25 . Subjects with AgP have features consistent with a Th1 bias, including Th1 cytokines in the GCF 26 and high levels of IFN‐γ–dependent IgG2 in their sera and GCF 19,27,28 . Barbour et al 29 reported that dendritic cells (DCs) spontaneously emerge in cultures of AgP monocytes and that monocyte‐derived DCs selectively promote IgG2 production.…”

Oral Delivery of a Probiotic Induced Changes at the Nasal Mucosa of Seasonal Allergic Rhinitis Subjects after Local Allergen Challenge: A Randomised Clinical Trial

“…IL-1 can enhance mast cell cytokine secretion and histamine release and studies in mice suggest its contribution to the pathogenesis of allergic rhinitis [14] . IL-1 and IL-1R regulation may therefore be an important contributory factor to the inflammation that occurs with allergen exposure [15] . It has been shown that soluble IL-1RII binds IL-1β to generate a composite binding surface to recruit soluble IL-1 receptor accessory protein (sIL-1RAcP) that serves to increase the affinity of sIL-1RII for IL-1β [16] while also stabilizing the [IL-1+IL-1RII] complex [17] .…”

Associations and interactions of genetic polymorphisms in innate immunity genes with early viral infections and susceptibility to asthma and asthma-related phenotypes

“…5 The genes of the IL-1R/TLR pathways are widely expressed in different cell types in the human lung. 6 The IL-1R subgroup has been implicated in the development of atopy and asthma, [7][8][9] and genetic associations with atopic diseases have been reported. 8 Single nucleotide polymorphisms (SNPs) of TLR2, 10,11 TLR4, 11 TLR6, 12 TLR9, 11,13 and TLR10 14 have also been reported to be associated with asthma or allergic diseases.…”