Ask about this productRelated genes to: IL18 antibody
- Gene:
- IL18 NIH gene
- Name:
- interleukin 18
- Previous symbol:
- -
- Synonyms:
- IGIF, IL1F4, IL-1g, IL-18
- Chromosome:
- 11q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-25
- Date modifiied:
- 2015-07-06
- 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: IL18 antibody
Related articles to: IL18 antibody
- Cardiopulmonary bypass (CPB) induces a systemic inflammatory response that may contribute to postoperative organ dysfunction. However, the effects of pulsatile and non-pulsatile CPB on the inflammatory response remain incompletely understood. This study investigated the perioperative dynamics of interleukin (IL)-1β, IL-18, and IL-18 binding protein (IL-18BP), as pre-specified secondary inflammatory biomarker analysis of a prospective, multicentric, randomized trial (ISRCTN11243508), in patients undergoing cardiac surgery with pulsatile or non-pulsatile CPB and evaluated their relationships with routine inflammatory and myocardial injury biomarkers. In this study 142 patients undergoing elective cardiac surgery were randomized to pulsatile (Group P) or non-pulsatile (Group NP) CPB, and 129 were analyzed (pulsatile, = 63; non-pulsatile, = 66). Blood samples were collected before surgery and at five postoperative time points. Plasma concentrations of IL-1β, IL-18, and IL-18BP were measured by ELISA. Leukocyte count, C-reactive protein (CRP), procalcitonin (PCT), high-sensitivity cardiac troponin I (hsTnI), and N-terminal pro-B-type natriuretic peptide (NT-proBNP) were also analyzed. The trial was powered for its primary outcome; for these secondary outcomes the achieved sample size had 80% power to detect between-group ratios of geometric means of approximately 1.27 (IL-18), 1.41 (IL-18BP) and 1.38 (IL-1β). Cardiac surgery with CPB induced a marked postoperative inflammatory response in both groups: leukocyte count, CRP, PCT, IL-18, IL-18BP, hsTnI and NT-proBNP increased significantly after surgery, whereas IL-1β remained essentially unchanged. In the pre-specified confirmatory comparison of postoperative peak concentrations, no biomarker differed significantly between groups. The 95% confidence intervals of this comparison exclude a pulsatile-flow effect on peak IL-18 larger than a 15% reduction or 19% increase, and on peak IL-18BP larger than a 26% reduction or 20% increase. A supporting mixed model for repeated measures showed no differential trajectory over time for any biomarker; its confidence intervals for the average postoperative effect were narrower (approximately ±10% for IL-18 and -9% to +15% for IL-18BP). The only exception was the leukocyte count, which was approximately 10% higher throughout the postoperative period in Group NP, without a differential trajectory shape. This pre-specified secondary analysis of a randomized trial found no evidence that pulsatile CPB reduces the early postoperative inflammatory or myocardial-injury response compared with non-pulsatile CPB for any of the eight biomarkers studied, apart from a modest difference in leukocyte count that did not survive correction for multiple comparisons. The confidence intervals obtained exclude only moderate-to-large between-group differences in IL-18 and IL-18BP; smaller true differences remain compatible with the data and cannot be ruled out at this sample size. These findings should not be interpreted as evidence of biochemical equivalence between pulsatile and non-pulsatile CPB, but they do not support a clinically important early anti-inflammatory advantage of pulsatile perfusion in this population. - Source: PubMed
Publication date: 2026/09/17
Ljubačev AleksandraGrčić AntonijoBatičić LaraJenko MatejTaleska Štupica GordanaĆurko-Cofek BoženaŠestan MiaLaškarin GordanaKnežević DanijelDamić MarinoVujnović Đukić VlatkaMedved IgorŠoštarič MajaAntonič MihaZdravković MarkoSotošek Vlatka - Objective Chronic pancreatitis (CP) is a fibro-inflammatory syndrome characterized by irreversible tissue damage leading to exocrine and endocrine insufficiency, persistent pain, and an increased risk of pancreatic cancer. This study investigates the role of IL-18 in the activation process of pancreatic stellate cells (PSCs) and the progression of pancreatic fibrosis in CP. Materials and Methods A total of 69 CP and 32 normal pancreatic tissue samples were analyzed using qRT-PCR and IH) to assess IL-18R1 expression. Primary PSCs were isolated from murine pancreata and cultured. Effects of recombinant IL-18 on PSC activation were evaluated using qRT-PCR and flow cytometry. Additionally, the impact of IL-18 binding protein (IL-18BP) and IL-18R1 antibody on PSC activation was examined. Results IL-18R1 expression was significantly upregulated in CP tissues compared to normal pancreatic tissues, correlating with fibrosis severity. Cultured PSCs showed increased α-SMA and IL-18R1 expression over time, indicating activation. Treatment with recombinant IL-18 induced a dose-dependent increase in α-SMA expression, confirming PSC activation. Furthermore, cultured PSCs secreted IL-18, suggesting an autocrine activation mechanism. IL-18BP and IL-18R1 antibody treatments reduced PSC activation, underscoring IL-18's regulatory role. Conclusion Upregulation of IL-18R1 and its correlation with fibrosis severity in CP highlights IL-18's significant role in PSC activation and pancreatic fibrosis. These findings suggest that targeting the IL-18/IL-18R1 axis could be a promising therapeutic strategy to mitigate pancreatic fibrosis in CP, offering potential new avenues for treatment. - Source: PubMed
Publication date: 2026/09/12
Aghamaliyev UghurLi ZhiqiangSirtl SimonMunker StefanWeniger MaximilianYu XiaoLevis ArthurBrohawn Philip ZAstanova BanuTan KeithCeyhan Güralp OnurBozkurt MerveFriess HelmutWerner JensBazhin AlexandrD'Haese Jan GIlmer MatthiasRenz Bernhard W - Cytokines (CYT) are regulators of the acute phase immune response (APR) to inflammation and trauma. The purpose of this work was to assess blood level correlations of various CYTs; interleukin-18 (IL-18), IL-18 binding protein (IL-18BP), free interleukin 18 (IL-18F) numerical rating pain scale (NRS) and number of analgesic doses (NAD) following surgery in patients undergoing laparoscopic cholecystectomy (LC) or minilaparotomy cholecystectomy (MC). - Source: PubMed
Eskelinen MattiKuosmanen ViiviSelander TuomasKaarniranta KaiSaimanen IinaEskelinen Maaret - Interleukin-18 (IL-18) is a pleiotropic cytokine of the IL-1 family that has an important role in antitumour and antiviral immunity. Growing interest in its therapeutic potential has led researchers to explore strategies that harness IL-18 to modulate the tumour microenvironment. For example, engineered T cells are being armoured with IL-18 to enhance adoptive cell therapies and strengthen other immunotherapy approaches. As these strategies move towards clinical application, a key translational challenge is identifying the molecular mechanisms that influence treatment response and resistance, crucial for guiding trial design and patient selection across tumour types. This Review revisits the fundamental biology of IL-18, including its origins, cellular sources and regulatory networks, particularly those involving IL-18 binding protein (IL-18BP) and IL-37. We discuss how IL-18 promotes interferon-γ (IFNγ) production within the tumour microenvironment, supporting M1-like macrophage polarization, CD8 cytotoxic T cell and CD4 T helper 1 cell responses, natural killer cell activity and durable T cell memory. We also discuss preclinical models of IL-18 delivery, including dendritic cell platforms and cellular therapies, and highlight emerging strategies such as IL-18BP blockade and IL-18-secreting CAR T cells. Finally, we review results from early clinical studies and outline key challenges for translation, including the dual protumour and antitumour roles of IL-18. - Source: PubMed
Publication date: 2026/07/16
Sharma AkshatBishara Gina GOlejniczak Scott HOhm Joyce EBrentjens Renier JGupta Ajay - Immune checkpoint inhibitors have revolutionized cancer therapy, yet a substantial proportion of patients exhibit primary or acquired resistance. Immunocytokines offer a strategy to enhance antitumor immunity by delivering cytokine signals selectively to the tumor microenvironment. Here, we describe the immunoconjugate anti-programmed cell death protein 1 (PD-1)-interleukin (IL)-18 (aPD1-IL18), designed to couple PD-1-blockade with localized IL-18-mediated immune activation. - Source: PubMed
Publication date: 2026/07/14
Oelgarth NicoleMartin KeaJunker FabianSerger ClaraHerr CaoimheBuchi MélanieGremlich LilianFusi IreneFürst JonasHerzig PetraMoosmann PhilippHeinzelmann-Schwarz ViolaMertz Kirsten DRosenberg RobertSchaeuble KarinCarralot Jean-PhilippeLuu Thuy TKreft BertoltPattabiraman VijayaZippelius Alfred