IL18BP _ IL18BPa Antibody
- Known as:
- IL18BP _ IL18BPa Antibody
- Catalog number:
- 10357-MM02
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- IL18BP _ IL18BPa Antibody
Related genes to: IL18BP _ IL18BPa Antibody
- Gene:
- IL18BP NIH gene
- Name:
- interleukin 18 binding protein
- Previous symbol:
- -
- Synonyms:
- IL18BPa
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-21
- Date modifiied:
- 2016-10-05
Related products to: IL18BP _ IL18BPa Antibody
Related articles to: IL18BP _ IL18BPa Antibody
- Sickle cell disease (SCD) is one of the most common monogenic diseases in the world. This blood disorder damages all organs and is associated with severe systemic complications and increased mortality risk. Predicting SCD severity is currently difficult due to a lack of biomarkers. Here, we measured 5,411 plasma proteins in 376 SCD patients and 103 non-SCD participants to find new predictors of SCD mortality. We used protein signatures of mortality that were developed in non-SCD populations to calculate predicted mortality risk scores in our SCD dataset. The mortality scores were higher in SCD patients than non-SCD participants (P-value=3.7x10-10) and were associated with increased mortality in SCD patients (risk factors-adjusted hazard ratio [HR] and 95% confidence interval=2.2 [1.3-3.6], P-value=0.0032). The mortality scores correlated with several clinical variables (e.g. white blood cell count, hemoglobin concentration) and complications (e.g. leg ulcers, stroke) that are clinically relevant yet insufficient individually to predict SCD mortality. In addition to the protein signatures, we found 499 plasma proteins that associate with mortality in SCD patients (false discovery rate £5%), including many proteins involved in inflammatory responses such as the IL18 signaling cascade (IL18R1, IL18BP, IL18). Finally, we estimated biological age in SCD patients and non-SCD participants using the plasma proteome data. We confirmed that SCD patients age prematurely (+6.0±5.4 years older than their chronological age) and found that brain biological age positively associates with past occurrences of stroke. Altogether, our results support the use of the plasma proteome to monitor and predict clinical severity in SCD. - Source: PubMed
Publication date: 2026/03/19
Chignon ArnaudZaouali YosrGalacteros FredericBartolucci PabloLettre Guillaume - Interleukin-18 (IL-18) is a member of the IL-1 cytokine family with significant homology to IL-1β. New emerging evidence indicates that IL-18 acts as a pivotal molecular bridge connecting innate and adaptive immunity, functioning through tightly regulated mechanisms involving inflammasome-dependent and -independent proteolytic processing. The activity of IL-18 is primarily maintained by IL-18 binding protein (IL-18BP), which neutralizes IL-18 under physiological conditions. However, dysregulations in the IL-18/IL-18BP axis result in excessive IL-18 bioactivity, driving tissue inflammation and damage closely associated with autoimmune pathogenesis. Herein, we review recent advances in IL-18 biology and its expanding roles in the development of various autoimmune diseases. The molecular mechanisms by which IL-18 mediates organ-specific pathology are discussed to highlight its diverse effector functions across different autoimmune conditions. In addition, we evaluate emerging therapeutic approaches targeting the IL-18 pathway, with a focus on their potential and challenges in translational clinical research. - Source: PubMed
Publication date: 2026/03/16
Zhao YueTang YuanZhu XiaoxiaHou YunxiaLi HongbinCiccia FrancescoZou HejianLu Liwei - Mevalonate kinase deficiency (MKD) is a rare monogenic autoinflammatory disorder characterized by recurrent fever episodes driven by dysregulated IL-1β secretion. Mutations in the MVK gene cause enzymatic defects resulting in a shortage of geranylgeranyl pyrophosphate, leading to a lowering of the threshold for pyrin inflammasome activation. - Source: PubMed
Publication date: 2026/03/09
van Heusden Niels SCuijpers IsaMeijer NilsPieren DaanMarkovska AngelaGabay CemGirard CharlotteKoné-Paut IsabelleVastert BasHamann DörteJans JudithVan Nieuwenhove ErikaFrenkel JoostBoes Marianne - Metabolic stress in obesity and diabetes activates innate immunity. Chronic IL-1β antagonism improves insulin secretion in type 2 diabetes. However, it is unclear how rapidly this effect occurs, whether it is also present in individuals with prediabetes, and if IL-1β influences GLP-1 secretion. Therefore, we acutely antagonized IL-1β in patients with prediabetes overnight. Two injections of anakinra significantly reduced total leucocyte count ( < 0.001), neutrophils ( < 0.001), monocytes ( = 0.006), and CRP ( = 0.030) compared with placebo. Lymphocytes were slightly elevated ( = 0.045). A mixed meal tolerance tests showed a trend toward increased early insulin ( = 0.11) and GLP-1 responses ( = 0.055), with GLP-1 ( = 0.020) and glucagon ( = 0.003) levels being significantly higher at 120 min under anakinra. Cytokine analysis showed elevated baseline concentrations of IL-1β, IL-6, and IL-1Ra under anakinra (all < 0.001), with IL-1β ( < 0.001) and IL-18BP ( = 0.048) decreased, and IL-6 increased ( = 0.059) after 60 min. Therefore, an acute injection of anakinra significantly reduces CRP and leucocyte counts in individuals with prediabetes, indicating effective innate immune modulation even after immediate treatment. Despite seeing no significant improvements in insulin secretion or glucose metabolism, we observed a trend toward earlier insulin secretion, along with increased release of IL-6 and GLP-1. We conclude that acute IL-1 antagonism dampens systemic inflammation in prediabetes, with the potential to improve insulin secretion via IL-6-induced GLP-1. Acute IL-1 blockade with anakinra markedly reduced CRP and leukocyte counts within 12 h, demonstrating rapid anti-inflammatory efficacy. Anakinra induced a trend toward earlier insulin secretion and significantly increased postprandial IL-6 and GLP-1 levels. The study demonstrates that even short-term IL-1 blockade can modulate both immune and incretin responses in prediabetes. Early IL-1β antagonism may represent a preventive, anti-inflammatory approach to preserve GLP-1 secretion and β-cell function in individuals with prediabetes. - Source: PubMed
Publication date: 2026/03/04
Fischer Justus SHepprich MatthiasCattaneo MarcoSeeger LuciaDobler StefanieDonath Marc Y - Immune response evasion is one of the hallmark features of cancer, which is not only the basis for cancer progression and metastasis but also affects the clinical management of cancer. Tumor immune evasion is mainly attributed to the dynamic and immunosuppressive tumor microenvironment (TME), which is regulated by a complex system including immunosuppressive cells and cytokines. Interleukin-18 (IL-18) is an important cytokine that plays a multifaceted role in immune system regulation, and its function is strictly regulated by the natural antagonist IL-18 binding protein (IL-18BP). IL-18 exhibits context-dependent immunoregulatory characteristics (acting as a "context resistor") during tumor occurrence and progression, which is closely related to cancer type, stage, and the signaling network of the tumor microenvironment. The multifaceted functions of IL-18 have been utilized in cancer treatment to reduce the phenomenon of immune escape of tumors. With the latest advancements in cancer research related to IL-18, it is necessary to integrate the latest research findings to deepen the understanding of the mechanism of tumor immune escape and promote the improvement of cancer treatment levels. This review will systematically elaborate on the action mode, core regulatory mechanism and key signaling pathways of IL-18 in tumor immune evasion, analyze the heterogeneity patterns associated with its context-dependent effects, comprehensively sort out the core obstacles in clinical translation, and at the same time, envision new precision treatment strategies based on IL-18 regulation. - Source: PubMed
Publication date: 2026/02/12
Li ShuaiGao ChenxiaZhao HongyuWang DidiLiu Shuang