IL1R1 _ CD121a Antibody
- Known as:
- IL1R1 _ CD121a Antibody
- Catalog number:
- 10126-RP01
- Product Quantity:
- 200
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- IL1R1 _ CD121a Antibody
Related genes to: IL1R1 _ CD121a Antibody
- Gene:
- IL1R1 NIH gene
- Name:
- interleukin 1 receptor type 1
- Previous symbol:
- IL1R, IL1RA
- Synonyms:
- D2S1473, CD121A
- Chromosome:
- 2q11.2-q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-27
- Date modifiied:
- 2018-02-13
Related products to: IL1R1 _ CD121a Antibody
Related articles to: IL1R1 _ CD121a Antibody
- Leptin, an adipose tissue-derived hormone, regulates multiple aspects of hepatic physiology beyond its well-established metabolic functions. Accumulating evidence indicates that leptin influences hepatocyte viability, yet its role in endotoxin-induced liver injury remains incompletely understood. In this study, we investigated the sensitizing effect of leptin on lipopolysaccharide (LPS)-induced hepatocyte toxicity. We found that leptin at a physiologically relevant concentration (20 ng/ml) markedly sensitized hepatocytes to LPS-stimulated apoptosis, whereas leptin or LPS alone exerted no significant effect. This sensitizing effect was not observed in hepatocytes derived from hepatocyte-specific interleukin-1 receptor type 1 (IL1R1)-deficient mice, indicating a critical role for IL-1R1 signaling in these effects. Essentially similar results were obtained for apoptotic cell death, as demonstrated by Annexin-V/7-AAD staining and altered expression of key biochemical markers of apoptosis. Moreover, leptin/LPS-induced apoptosis was significantly attenuated by neutralization of IL-1β, but not by an IL-1α antibody. The in vitro observations were further validated in vivo, where combined administration of leptin and LPS induced pronounced liver injury, as evidenced by elevated serum AST/ALT levels and enhanced apoptotic signaling, all of which were substantially prevented in hepatocyte-specific IL1R1 knockout mice. Additionally, co-treatment with leptin and LPS elicited robust inflammatory cytokine production under both in vitro and in vivo conditions; this effect was absent in IL1R1-deficient models. Notably, combined leptin and LPS stimulation promoted Th17 differentiation from naïve T cells, leading to B cell activation and enhanced antibody production in an IL1R1-dependent manner. Collectively, these results suggest that leptin sensitizes hepatocytes to endotoxin-induced apoptosis via IL-1β signaling-dependent mechanism, thereby amplifying hepatic inflammation and adaptive immune activation. - Source: PubMed
Publication date: 2026/04/20
Baral AnandaPark Pil-Hoon - Metabolic disturbances, particularly glucose imbalances, are common in sepsis and are strongly associated with increased mortality. However, the mechanisms underlying glucose dyshomeostasis remain poorly understood. Here, we revealed the role of triggering receptor expressed on myeloid cells 2 (TREM2) in regulating glucose metabolism during sepsis. Macrophage-specific TREM2 deficiency significantly increased the level of abdominal IL-1, which is predominantly released by pyroptotic peritoneal macrophages. IL-1 then acts on IL-1R1 receptors on pancreatic islet β-cells, promoting insulin release and inducing hypoglycemia. Transfusing TREM2-overexpressing macrophages and administering glucose solutions can restore glucose homeostasis and improve sepsis outcomes in mice. In summary, our study reveals a mechanism by which TREM2 orchestrates glucose metabolism during sepsis and highlights the potential of TREM2 as a therapeutic target for sepsis. - Source: PubMed
Publication date: 2026/03/19
Wu ZeHuaWang XueKeRen YiChaoShen LiHuaPan YiHangZhang YanFan JiaQianShu QiangFang XiangmingChen QiXing - Osteoarthritis (OA) is a prevalent degenerative joint disease with an unclear molecular pathogenesis. B4GALT1 has been implicated in various pathological processes, but its role and mechanism in OA remain largely unexplored. - Source: PubMed
Publication date: 2026/04/17
Ma WeibangOuYang DongXu ZheLuo WeiTian GuangJiang NingLiu ChenZhang RuguoYu Qiao - Interleukin (IL)-38 has been identified as an anti-inflammatory cytokine; however, its specific role in temporomandibular joint (TMJ) synovial inflammation and the identity of its functional receptors remain elusive. This study aimed to investigate the therapeutic efficacy of IL-38 in TMJ synovial inflammation and to elucidate its potential receptor mechanisms. - Source: PubMed
Publication date: 2026/04/18
Luo PingLv XueliangHui JifangQiao Hu - Brain injury elicits complex tissue responses that are dynamically regulated between activation and resolution, yet the mechanisms that govern this balance remain elusive. We show that acute injury evokes focal extracellular ATP events (Inflares) with characteristic spatiotemporal signatures that scale quantitatively with injury severity, suggesting a glial mechanism for damage calibration. We further reveal that microglia exert negative feedback on Inflares by tuning interleukin (IL)-1β output based on extracellular ATP levels and cellular state. The IL-1β signal is directly received by astrocytes through IL-1R1 and intracellular Ca-calcineurin signaling, where it converges with injury input to shape Panx1-dependent ATP release. These bidirectional interactions form a reciprocal glial circuit that enforces a balanced injury response, while disrupting the circuit destabilizes the dynamic control, impairing the cellular reactivity and worsening early injury outcomes. Our findings uncover a glial circuit and molecular players that dynamically regulate tissue injury responses. - Source: PubMed
Publication date: 2026/04/15
Luan PengweiJia JianmingChen YueXi FengxueSchwarcz Anett DJiang XiujieKörnyei ZsuzsannaKalmár BalázsWang YaDénes ÁdámJing Miao