Proteins IL-16 , Human
- Known as:
- Proteins Interleukin-16 , Human
- Catalog number:
- C045
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins IL-16 Human
Related genes to: Proteins IL-16 , Human
- Gene:
- IL16 NIH gene
- Name:
- interleukin 16
- Previous symbol:
- -
- Synonyms:
- LCF, IL-16, prIL-16, HsT19289, FLJ42735, FLJ16806
- Chromosome:
- 15q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-25
- Date modifiied:
- 2016-10-05
Related products to: Proteins IL-16 , Human
Related articles to: Proteins IL-16 , Human
- Oral inflammatory diseases affect nearly half of all humans, yet mechanisms underlying rapidly-destructive inflammation remain poorly understood. We compared peri-implantitis with moderate- and high-grade periodontitis using integrated microbial and single-cell sequencing (>967,169-cells; single-cell RNA-seq, spatial proteotranscriptomics). Laser capture microdissection with compartmental microbiome analysis revealed reduced bacterial load and diversity in peri-implantitis. Expansion of the Human Periodontal Atlas with peri-implantitis single-cell RNA-seq data (36-samples; 121,395 cells) identified CD34 vascular endothelial cell (VEC) rarefaction and oxidative stress, hypoxia, and NAD⁺ metabolism-associated transcriptional programs enriched in a TNFRSF6B⁺/ICAM1⁺ post-capillary venule (PC-VEC) subpopulation. NAD⁺-consuming ectoenzyme CD38 was selectively enriched and orthogonally confirmed by spatial transcriptomics (6-samples; 283,377-cells) and proteomics (23-samples; 562,397-cells). Spatial neighborhood analyses demonstrated CD38⁺-high PC-VEC expansion, closer proximity, and higher IL16-CD4 T cell signaling in peri-implantitis. Matched high-grade periodontitis biopsies confirmed spatially restricted CD38⁺-VECs despite similar microbial burden, identifying endothelial vasculopathy underlying rapidly advancing oral inflammation and a potential therapeutic axis. - Source: PubMed
Publication date: 2026/05/08
Easter Quinn THuynh Khoa L AStolf Camila SchmidtXie JialiuMatuck Bruno FHasuike AkiraAlvarado-Martinez ZabdielKim William SChen ZhaoxuRibeiro Apoena AguiarPareek NiveditaAzcarate-Peril Andrea MWu DiCasarin RenatoKo Kang ILiu JinzeByrd Kevin M - Elevated remnant lipoproteins are a causal risk factor for atherosclerotic cardiovascular disease. We tested the hypothesis that low-grade inflammation can explain part of the increased risk of peripheral artery disease (PAD) and myocardial infarction conferred by elevated remnant lipoproteins; we also explored the causal effect of genetically elevated remnant cholesterol on inflammatory cytokine levels. - Source: PubMed
Publication date: 2026/05/01
Wadström Benjamin NWulff Anders BPedersen Kasper MNordestgaard Børge G - Ovarian cancer is the most lethal gynecological malignancy worldwide, largely due to late diagnosis and lack of effective population-level screening tools. Inflammatory cytokines regulate proliferation, apoptosis, angiogenesis, and immune surveillance, making inherited variation in cytokine pathways biologically plausible determinants of ovarian cancer susceptibility and progression. Since the early 2000s, numerous candidate-gene studies have evaluated polymorphisms of genes such as the interleukin () families, tumor necrosis factor alpha (), transforming growth factor beta 1 (), and components of the nuclear factor kappa B () signaling pathway and adhesion pathways, across diverse populations. In this review, we summarize these potential markers to give readers an overview showing accumulated evidence supports a coherent model in which genetically modulated inflammation is an integral driver of epithelial ovarian carcinogenesis. Collectively, studies reveal recurrent patterns of risk-increasing and risk-protective variants. Risky genotypes predicted to enhance pro-inflammatory, pro-angiogenic, or immunosuppressive signaling include rs16944 CC, rs1800795, rs2227306 TT, rs1126647 TT, rs11556218 GT/GG, rs4778889 CT/CC, rs10889677 AC/CC, rs4758680 CA/AA, rs28372698 TT, rs1800629 GA/AA, and peroxisome proliferator-activated receptor gamma () rs1801282 CG genotypes. Conversely, protective variants tend to dampen inflammatory tone or rebalance cytokine networks, including rs17561 GT/TT, rs4848300 CT/CC, rs3783553 insertion/insertion, rs7596684 CT/CC, rs1880242 GT/TT, rs7977932 CG/GG, rs1800469 CT/TT, selectin E () rs5361 AC, intercellular adhesion molecule 1 () rs5498 AG genotypes and specific haplotypes. Beyond risk , several polymorphisms appear predictive of clinical features, including tumor stage, cytoreductive resectability and recurrence, highlighting potential prognostic relevance. Notably, associations are often population-specific, reflecting differences in allelic frequencies and linkage disequilibrium across ethnic groups, underscoring the need for cross-ethnic replication. Further investigations may ultimately enable further improved the prevention, early detection, and personalized management of ovarian cancer. - Source: PubMed
Chang Wen-ShinTsai Chia-WenChen Jaw-ChyunWang Yun-ChiBau DA-Tian - To evaluate histopathological renal response in re-biopsy after induction therapy and to correlate with the Target Renal Response (TRR) and secondary objective: to correlate serum and urinary biomarkers with creatinine, 24-hour proteinuria, histological class, activity index and chronicity index. - Source: PubMed
Publication date: 2026/04/27
Egypto Danielle ChristinneReis-Neto Edgard Torres DosCarlesso Guilherme PereiraMoura Luiz AntonioAndrade Luis E CCalderaro DeboraSato Emilia Inoue - Intermittent hypoxia (IH), a hallmark feature of obstructive sleep apnea (OSA), is associated with a range of physiological alterations that contribute to metabolic dysfunction and insulin resistance. IH induces adipose tissue inflammation and macrophages may play a key role in such homeostatic derangements. To examine the role of monocytes/macrophages in OSA, CD11b-diphtheria toxin receptor transgenic (DTR) mice were treated with diphtheria toxin (DT) to selectively eliminate these cells and assess changes in the metabolic function of IH-exposed mice. Transgenic homozygous male and female DTR mice were exposed to IH or room air (RA) for 6 weeks during which insulin sensitivity and other metabolic measures were assessed. Immunofluorescence analysis was performed for CD11b+ expression in metabolic tissues such as liver and visceral white adipose tissue (vWAT). Gene expression patterns associated with senescence-associated secretory phenotypes (SASPs) as well as adipokines and cytokines were evaluated. Depletion of CD11b+ cells in mice exposed to IH resulted in significant improvements in metabolic function and insulin sensitivity. Macrophage infiltration, assessed by F4/80 or CD11b immunostaining, was significantly reduced following CD11b ablation in IH exposed mice compared with controls in both males and females. Moreover, CD11b+ cell ablation led to a marked decrease in SASPs markers (p16 and Il-16) at both transcriptional and protein levels in vWAT and liver. Thus, depletion of CD11b+ cells in mice exposed to IH can significantly modulate the inflammatory response in multiple metabolic organs including visceral adipose tissues and markedly mitigate metabolic dysfunction. Targeted interventions aimed at some of the functional roles played by activated CD11b+ cells or SASPs within metabolic organs may improve metabolic regulation in OSA patients. - Source: PubMed
Publication date: 2026/04/27
Khalyfa AbdelnabyAhmed SarfrazQiao ZhuanhongLamichhane RajanGozal David