IL-1R8

Last update 08 May 2025

Basic Info

Synonyms

IL-1R8, SIGIRR, single Ig and TIR domain containing

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Introduction

Acts as a negative regulator of the Toll-like and IL-1R receptor signaling pathways. Attenuates the recruitment of receptor-proximal signaling components to the TLR4 receptor, probably through an TIR-TIR domain interaction with TLR4. Through its extracellular domain interferes with the heterodimerization of Il1R1 and IL1RAP.

100 Clinical Results associated with IL-1R8

100 Translational Medicine associated with IL-1R8

0 Patents (Medical) associated with IL-1R8

271

Literatures (Medical) associated with IL-1R8

01 Jul 2025·Fish & Shellfish Immunology

A novel double Ig interleukin-1 receptor-related molecule from Apostichopus japonicus alleviates Vibrio splendidus-induced inflammation

Article

Author: Zhu, Si ; Ye, Wenwen ; Li, Chenghua ; Lv, Zhimeng

In vertebrates, the single immunoglobulin (Ig) interleukin-1 receptor-related molecule, SIGIRR, plays a role in controlling inflammatory responses. Its invertebrate homologous double Ig interleukin-1 receptor-related molecule, DIGIRR, is little known. We report here the cloning of a novel DIGIRR homologue in Apostichopus japonicus, named AjDIGIRR, using rapid amplification of cDNA ends (RACE). Gene structure analysis revealed that AjDIGIRR contains a conserved intracellular TIR domain that differs from SIGIRR and IL-1R by having a different number of extracellular Ig domains. Subcellular localization analysis showed that, unlike fish DIGIRR, which is cytoplasmic, AjDIGIRR was membrane-associated and had increased expression 24 h after infection. In vertebrates, two amino acid sites in the TIR domains of IL-1R family members, Ser and Arg-Tyr, are conserved and are required for receptor signaling. Sequence alignment revealed that the primary signaling site, S279, is conserved in DIGIRR, whereas the signal activation site, Arg-Tyr536, is mutated to Gln-Gly359 in AjDIGIRR. To investigate AjDIGIRR's role in inflammation regulation, an in vivo inflammation model was established using Vibrio splendidus. Following bacterial challenge, AjDIGIRR mRNA expression in coelomocytes peaked at 6 h (1.92-fold increase) and remained elevated (1.63-fold increase) for up to 48 h, consistent with the inflammatory response. AjDIGIRR knockdown (0.26-fold) significantly exacerbated inflammation, as shown by HE staining, whereas overexpression (7.85-fold) markedly alleviated the inflammatory response. Under inflammatory conditions, AjDIGIRR overexpression reduced IL-17 expression by 29 % compared to the V. splendidus-induced group. These findings suggest that AjDIGIRR is structurally and functionally more similar to mammalian SIGIRR than to fish DIGIRR. Acting as a key negative regulator, AjDIGIRR mitigates inflammation by downregulating IL-17 expression.

01 May 2025·Journal of Controlled Release

AAV9-delivery of interleukin-37b gene prevents recurrent herpetic stromal keratitis via the SIGIRR pathway in mice

Article

Author: Zhu, Xiaomin ; Liu, Ye ; Cai, Yurong ; Qin, Qin ; Wu, Jing ; Chen, Deyan ; Lyu, Ruining ; You, Qiao ; Qian, Yajie ; Liu, Xiaoqian ; Wang, Chenchen

Ocular herpes simplex virus type I (HSV-1) infection can lead to herpes stromal keratitis (HSK), a condition that may recur throughout a person's life and often results in progressive corneal scarring, which ultimately causes visual impairment. Since existing antiviral agents are ineffective against recurrent HSK, we aimed to explore a strategy to prevent or control recurrent HSK. Adeno-associated virus (AAV) delivery system can transduce target genes into corneal epithelial cells and establish long-term stable gene expression, and providing a promising approach for the prevention and management of recurrent HSK. In this study, interleukin-37 (IL-37), an anti-inflammatory factor, is identified as a therapeutic agent for recurrent HSK via the SIGIRR pathway. AAV9-IL-37bΔ1-45 gene therapy prevents recurrent HSK in HSV-1 latently infected mice and alleviates corneal injury in mice with HSK. In conclusion, our present study establishes a strong foundation for the prevention of recurrent HSK through AAV9-IL-37bΔ1-45 gene therapy.

01 Apr 2025·iScience

Neonatal gut microbiota succession in mice mapped over time, site, injury and single immunoglobulin interleukin-1 related receptor genotype

Article

Author: Attard, Mark Ivan ; Morowitz, Michael ; Umar, Shahid ; Ahmed, Ishfaq ; Xuan, Hao ; Yu, Wei ; Zhong, Cuncong ; Sampath, Venkatesh ; Rogers, Mathew Brian

Microbial succession during postnatal gut development in mice is likely impacted by site of sampling, time, intestinal injury, and host genetics. We investigated this in wild-type and Sigirr transgenic mice that encode the p.Y168X mutation identified in a neonate with necrotizing enterocolitis (NEC). Temporal profiling of the ileal and colonic microbiome after birth to weaning revealed a clear pattern of progression from a less diverse, Proteobacteria/Escherichia_Shigella dominant community to a more diverse, Firmicutes/Bacteroidetes dominant community. Formula milk feeding, a risk factor for necrotizing enterocolitis, decreased Firmicutes and increased Proteobacteria leading to enrichment of bacterial genes denoting exaggerated glycolysis and increased production of acetate and lactate. Sigirr transgenic mice exhibited modest baseline differences in microbiota composition but exaggerated formula feeding-induced dysbiosis, mucosal inflammation, and villus injury. Postnatal intestinal microbiota succession in mice resembles human neonates and is shaped by developmental maturity, ileal vs. colonic sampling, formula feeding, and Sigirr genotype.

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IL-1R8

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