Ask about this productRelated genes to: IL1RL2 antibody
- Gene:
- IL1RL2 NIH gene
- Name:
- interleukin 1 receptor like 2
- Previous symbol:
- -
- Synonyms:
- IL1R-rp2, IL1RRP2
- Chromosome:
- 2q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-17
- Date modifiied:
- 2016-10-05
Related products to: IL1RL2 antibody
Related articles to: IL1RL2 antibody
- The cardiovascular effects of coffee consumption remain debated, particularly regarding early-stage subclinical atherosclerosis. This study investigated the association between coffee intake, genetic predisposition, and the risk of subclinical coronary and carotid atherosclerosis in 24,835 participants from the Swedish CArdioPulmonary bioImage Study (SCAPIS). Coffee intake was assessed via self-reported questionnaires. Atherosclerosis was assessed via segment involvement score (SIS), coronary artery calcium score (CACS) and carotid plaque. Observational analysis showed no significant association between coffee consumption and SIS, CACS, or carotid plaques. However, both one-sample and two-sample (SCAPIS and UK Biobank) Mendelian randomization (MR) analyses showed an association between genetic predisposition to higher coffee consumption and increased SIS. Stratification analyses further explored differences in genetic associations across varying coffee consumption levels. Among individuals consuming coffee more than twice daily, two coffee consumption-associated single nucleotide polymorphisms (SNPs) in AHR and CYP1A1/CYP1A2 were correlated with SIS. Integrative metabolomics and proteomics analyses identified lipid-related metabolites (triglycerides, phospholipids, free cholesterol) and inflammation-related proteins (DLK1, IL1RL2, CCL17) associated with the genetic proxy of coffee consumption. These findings suggest that genetically influenced coffee consumption may be associated with coronary atherosclerosis risk in frequent coffee drinkers, although the underlying biological basis remains to be clarified. - Source: PubMed
Publication date: 2026/03/22
Qiao XiangyuToma Vanessa WilliamWang JingHerraiz-Adillo ÁngelSöderholm SimonBerglind DanielCalling SusannaDaka BledarMartinell MatsBergman FridaHenriksson PontusGhafouri BijarUlander MartinÖstgren Carl JohanCantù ClaudioZhong WenIredahl Fredrik - The recruitment and polarization of tumor-associated macrophages (TAMs) play a pivotal role in shaping the immunosuppressive tumor microenvironment in breast cancer. Interleukin-1 receptor accessory protein (IL1RAP), a critical co-receptor for IL-1 family cytokines, is emerging as a potential regulator of macrophage function, though its specific role in TAM biology remains to be explained. In this study, we investigated the impact of IL1RAP on macrophage recruitment and M2-like polarization. Initial bioinformatics analysis of public databases revealed a significant correlation between elevated IL1RAP expression in macrophages and signatures of immune suppression and poor prognosis in breast cancer. To functionally validate these findings, we performed IL1RAP knockdown in a murine macrophage cell line. Our results demonstrated that IL1RAP deficiency markedly impaired the migratory capacity of macrophages towards classic chemotactic stimuli. Furthermore, under M2-polarizing conditions, IL1RAP-knockdown macrophages exhibited a significantly attenuated M2 phenotype, as evidenced by the decreased expression of canonical M2 markers (e.g., Arg1, Mrc1) and reduced functional outputs. Collectively, our integrated approach combining bioinformatics and in vitro experimentation identifies IL1RAP as a novel regulator that potentiates both the recruitment and the M2 polarization of macrophages. These findings suggest that targeting the IL1RAP pathway could represent a promising therapeutic strategy for reprogramming the tumor-immune microenvironment by limiting pro-tumoral macrophage infiltration and polarization. - Source: PubMed
Publication date: 2026/02/16
Zhu WuchengPeng GaogeWu YiZhang LixingHe MingangXin BeibeiJin WeiSun Hefen - Age-related inflammation plays a pivotal role in osteoarthritis (OA) pathogenesis, but the mechanism is not fully understood. Here, we identify decreased IL-36 receptor antagonists (IL-36Ra) in epidermal keratinocytes from a premature-aged skin mice model, aged mice and patients. Decreased IL-36Ra leads to increased secretion of IL-36 agonists to serum and joints, which activates proinflammatory signaling and promotes senescence in chondrocytes and synovial fibroblasts, thereby aggravates OA progression. Deletion of IL-36Ra in keratinocytes exacerbates, whereas intra-articular inhibition of IL-36R signaling effectively attenuates OA progression in male mice. Moreover, we also generate microneedles loaded with mouse recombinant IL-36Ra protein or spesolimab, insert them directly into skin to sustainably inhibit IL-36R signaling, which both clearly attenuate OA progression in male mice. Overall, our results reveal that IL-36 agonists are age-related systemic inflammatory factors released from skin to joints and contribute to OA development, and targeting IL-36R signaling in aged skin with microneedles represents a promising disease-modifying approach. - Source: PubMed
Publication date: 2026/01/14
Chen DalinWang ChongYang ChangshengCheng QinweiChen LiangyuYang PanpanZou ZilinWang ZiningLi HonghaoXiao YunWu JunfengKe EeWang XiaogangHuang BinBai XiaochunLi Kai - Therapies for acute myeloid leukemia (AML) face formidable challenges due to relapse, often driven by leukemia stem cells (LSCs). Strategies targeting LSCs hold promise for enhancing outcomes, yet paired comparisons of functionally defined LSCs at diagnosis and relapse remain underexplored. We present transcriptome analyses of functionally defined LSC populations at diagnosis and relapse, revealing significant alterations in IL-1 signaling. Interleukin-1 receptor type I (IL1R1) and interleukin-1 receptor accessory protein (IL1RAP) were notably upregulated in leukemia stem and progenitor cells at both diagnosis and relapse. Knockdown of IL1R1 and IL1RAP reduced the clonogenicity and/or engraftment of primary human AML cells. In leukemic MLL-AF9 mice, Il1r1 knockout reduced LSC frequency and extended survival. To target IL-1 signaling at both diagnosis and relapse, we developed UR241-2, a novel interleukin-1 receptor-associated kinase 1 and 4 (IRAK1/4) inhibitor. UR241-2 robustly suppressed IL-1/IRAK1/4 signaling, including NF-κB activation and phosphorylation of p65 and p38, following IL-1 stimulation. UR241-2 selectively inhibited LSC clonogenicity in primary human AML cells at both diagnosis and relapse, while sparing normal hematopoietic stem and progenitor cells. It also reduced AML engraftment in leukemic mice. Our findings highlight the therapeutic potential of UR241-2 in targeting IL-1/IRAK1/4 signaling to eradicate LSCs and improve AML outcomes. - Source: PubMed
Publication date: 2025/12/19
Ho Tzu-ChiehLaMere Mark WKawano HirokiByun Daniel KLaMere Elizabeth AChiu Yu-ChiaoChen ChunmoWang Li-JuWang JianRamdas BaskarDokholyan Nikolay VCalvi Laura MLiesveld Jane LJordan Craig TSingh Rakesh KKapur ReubenBecker Michael W - Interleukin-1 receptor accessory protein (IL1RAP) is selectively expressed on both bulk blasts and leukemic stem cells (LSCs) in acute myeloid leukemia (AML), while its expression is virtually absent on normal hematopoietic stem cells (HSCs), making it an appealing target for chimeric antigen receptor (CAR) T cell therapy. - Source: PubMed
Publication date: 2025/11/12
Harada KaitoZhao DandanPark MisoChen FangXu YongfangZhang YiZhou YileParcutela BeaJewel YeadMunoz AshlieAmanam IdoroenyiNguyen Le Xuan TruongChen JianjunGhoda LucyForman Stephen JWilliams John CZhang BinMarcucci Guido