IL1R1

(redirected from IL1R)

IL1R1

A gene on chromosome 2q12 that encodes a cytokine receptor for interleukin alpha (IL1A), interleukin beta (IL1B) and interleukin 1 receptor, type I (IL1R1/IL1RA). After binding to IL1, it associates with the co-receptor IL1RAP to form the high-affinity interleukin-1 receptor complex, which mediates interleukin-1-dependent activation of NF-kappa-B, MAPK and other pathways. Signalling involves the recruitment of adapter molecules such as TOLLIP, MYD88, and IRAK1 or IRAK2 via the respective TIR domains of the receptor/co-receptor subunit.
References in periodicals archive ?
Association of IL1R polymorphism with HLA-B27 positive in Iranian patients with ankylosing spondylitis.
These MSU crystals are sensed by IL1R, TLR2, and TLR4, which then activate NLRP3 inflammasome leading to IL-1[beta] production [143,144].
The role of HO-1 in the process of immunomodulation involves stimulation of Treg and production of IL-10 [10, 16] and production of the IL1R (IL-1 receptor) antagonist as well as induction of mitochondrial biogenesis [16].
Tumor necrosis factor (TNF) receptor associated factors (TRAFs) play important roles in intracellular signal transduction of many receptor families such as the IL-1 receptors (IL1R) [22].
Therefore, mice lacking IL1R cannot sufficiently induce Th17 cells and do not contract EAE [63].
IL-[beta] directly activated LECs, via IL1R, to produce VEGF-C, thus, directly linking macrophage NLRP3 inflammasome activation with lymphangiogenesis.
Stimulation of the P2X7R also elicits the production of IL-1[beta] and its maturation via CatS and CASP1 [36], which can further increase microglia activation via the interleukin receptor IL1R [37] and it is also a key contributor in the hyperexcitability of the nociceptive dorsal horn neurons [14].
This would imply that proteolytic shedding of cytokines like TNF[alpha] also regulates immune cell migration, and this activity could be counterregulated by receptor shedding of TNFR, IL1R, or IL6R [97, 99, 100].
Pyrenocine A also may exert anti-inflammatory effects by decreasing a specific mRNA of factors, such as Cxcl1, Ccl2, Bcl2, Icam1, Ptges, and Tlr2 in the pretreatment procedure (Figure 7), as well as Icam1 and Il1r in the posttreatment procedure (Figure 8).