Interleukin-18 receptor 1 (IL18R1) also known as CD218 antigen-like family member A, CDw218a, IL1 receptor-related protein and CD218a, is an interleukin receptor of the immunoglobulin superfamily. IL18R1 is found expressed in lung, leukocytes, spleen, liver, thymus, prostate, small intestine, colon, placenta, and heart, and is absent from brain, skeletal muscle, pancreas, and kidney. High level of expression is found in Hodgkin disease cell lines. This receptor is specifically binds interleukin 18 (IL18), and is essential for IL18 mediated signal transduction. IL18R1 contains 3 Ig-like C2-type (immunoglobulin-like) domains and 1 TIR domain. It is a single-pass type I membrane protein. IFN-alpha and IL12 are reported to induce the expression of this receptor in NK and T cells. The increased expression of IL18R1 may contribute pathogenically to disease and is therefore a potential therapeutic target. The absence of a genetic association in the IL18R1 gene itself suggests regulation from other parts of the genome, or as part of the inflammatory cascade in multiple sclerosis without a prime genetic cause.
Interleukin 18 receptor accessory protein, also known as IL18RAP and CDw218b (cluster of differentiation w218b), is an accessory subunit of the heterodimeric receptor for IL18. This protein enhances the IL18 binding activity of IL18R1 (IL1RRP), a ligand binding subunit of IL18 receptor. The coexpression of IL18R1 and this protein is required for the activation of NF-kappaB and MAPK8 (JNK) in response to IL18. IL18RAP is required for the high affinity binding of interleukin 18 (IL-18) to its receptor complex. IL18RAP together with IL18R1 mediates IL-18-dependent activation of NF-kappa-B and JNK. Two putative isoforms of IL18RAP were detected and the ratios and total levels of these isoforms may contribute to the aetiology of coeliac disease. IL18R1 and IL18RAP polymorphisms have been found associated with diseases such as schizophrenia, HSV1 seropositivity and atopic asthma. Analysis of IL18R1 and IL18RAP SNPs in 5 European prospective cohorts suggests that the variability of these genes are unlikely to contribute to modulate the risk of CVD in European populations.
IL-18RAP is a single-pass type I membrane protein and contains two Ig-like C2-type domains and one TIR domain, IL18RAP can be induced by IFN-alpha and IL12 in nature killer cells and T-cells. The coexpression of IL18R1 and IL18RAP is required for the activation of NF-kappa B and JNK in response to IL-18.Defects in IL18RAP are associated with Coeliac disease.
The molecular features at the IL19 locus may modestly alter the establishment of HIV-1 infection. Interleukin (IL) 19, IL-20, and IL-24 belong to the IL-10 cytokine family and have been identified to play a role in the regulation of epidermal functions and inflammation. The expression of IL19 in biopsies of patients with active ulcerative colitis was increased compared with patients with quiescent ulcerative colitis and that colitis was attenuated in IL-19-deficient mice. The disruption of the epithelial barrier with dextran sodium sulfate leads to increased IL-19 expression. Attenuated colitis in IL-19-deficient animals was associated with reduced numbers of IL-6-producing macrophages in the inflamed colonic lamina propria. Microbial-driven expression of IL-19 by intestinal macrophages may contribute to the pathogenesis of inflammatory bowel disease.
Interleukin-1 alpha (IL1α) is a cytokine member of the interleukin-1 family. IL-1 consists of two distinct forms: IL1α and IL1β that recognize the same cell surface receptors but are distinct proteins with approximately 25% amino acid sequence identity. IL1α is constitutively produced by epithelial cells and plays an essential role in maintenance of skin barrier function. Upon stimulation, a wide variety of cells including osteoblasts, monocytes, macrophages can be induced to express IL1α. IL1α possesses a wide range of metabolic, physiological, haematopoietic activities, and is critically involved in the regulation of the immune responses and inflammatory responses.
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