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
- Type 2 diabetes mellitus (T2DM) is a multifactorial metabolic disease in which inflammatory mechanisms are involved in disease development and progression. Polymorphisms in cytokine-related genes may influence susceptibility to T2DM, yet evidence in Vietnamese individuals remains scarce. This study was designed to investigate whether IL16 rs11556218 and IL1B rs16944 are associated with T2DM in Kinh Vietnamese adults. - Source: PubMed
Publication date: 2026/09/28
Lam Quynh AiPhan Hen HuuLe Linh Hoang GiaDo Minh Duc - Systemic inflammation contributes to the pathobiology of multiple sclerosis (MS), yet serum biomarker data from Middle Eastern populations remain limited. This study evaluated serum levels of IL-6, IL-16, IL-18, and IL-36 in Saudi adults with MS compared with matched healthy controls and examined associations with disease duration, phenotype, treatment, and disability. This single-center, cross-sectional, matched case-control study enrolled 26 MS patients and 26 age- and sex-matched controls. Serum cytokines were measured by ELISA. Disability was assessed using EDSS and the Timed 25-Foot Walk (T25FW). Matched comparisons used Wilcoxon signed-rank tests; subgroup comparisons used Wilcoxon rank-sum or Kruskal-Wallis tests; associations used Spearman's correlation. No correction for multiple comparisons was applied given the exploratory design. All four interleukins were higher in MS patients than in controls ( < 0.001). Age correlated with EDSS (r = 0.573, = 0.002) and T25FW (r = 0.464, = 0.014). Only IL-6 showed a notable correlation with disability, with T25FW (r = 0.53, = 0.008) and, weaker, EDSS (r = 0.38, = 0.052); IL-18 showed a weak, non-significant correlation with T25FW (r = 0.35, = 0.126); IL-16 and IL-36 showed no relevant associations. IL-16 was higher in newly diagnosed than in long-standing cases ( = 0.012); no differences by phenotype or treatment were observed for any marker. Serum IL-6, IL-16, IL-18, and IL-36 were elevated in Saudi MS patients versus controls. IL-6 alone showed a modest, unadjusted association with disability, supporting its evaluation as a candidate biomarker in larger, longitudinal, covariate-adjusted cohorts. These findings are hypothesis-generating and should not be interpreted as evidence of independent or clinically actionable biomarker utility. - Source: PubMed
Publication date: 2026/09/01
Alrahimi JehanMualla YaraAlhebshi AlawiahAlnajashi Hind AZaher Kawther - Endometriosis is a multifaceted disease, causing debilitating pelvic pain in some patients, while being completely asymptomatic in others. The pathophysiology of endometriosis pain is not well understood and poorly correlated to stage. We hypothesized that this clinical heterogeneity may be explained by examining differences in gene expression. We performed RNA sequencing of 27 formalin-fixed, paraffin-embedded peritoneal biopsies from 9 symptomatic (Sx) and 10 asymptomatic (ASx) subjects. 890 genes were differentially expressed between Sx and ASx samples. Of these, the most significant including genes involved inflammatory signaling (IL16, IL17RA, JAK3, SMPD3, RELT), cell adhesion (OLFML1, CDON, VCAN), and neuromodulation (SEMA6D, ADRA2C, SLC7A5). Gene Set Enrichment Analysis identified functional enrichment in 22 gene ontology (GO) pathways, of which 7 represented immunologic pathways. Weighted Gene Correlation Network Analysis (WGCNA) identified 11 co-expression modules significantly correlated with symptomaticity, including one module strongly enriched for immunologic/inflammatory functions. Of all molecules identified as associated with pain, IL16 expression also correlated with symptom severity when cases were stratified into mild vs. severe pain based on clinical criteria. These findings suggest that endometriotic lesions of symptomatic subjects are characterized by distinct molecular signatures, including altered expression of inflammatory pathways, highlighting potential mechanisms underlying symptom variability and identifying candidate pathways for future therapeutic interventions. - Source: PubMed
Publication date: 2026/09/10
Mamillapalli RamanaiahLi Howard JApelian ShantKumar MonishWang Sarah FPondugula NishitaCampos Gabriela de QueirozSayeed SumaiyaCho YongheeTaylor Hugh S - Eosinophilic esophagitis (EoE) is a chronic immune-mediated disorder of the esophagus. However, the T-cell transcriptional programs distinguishing active disease from remission remain incompletely understood. In this study, we applied single-cell RNA sequencing to esophageal biopsies obtained from normal subjects and patients in remission or with active EoE, to characterize T-cell heterogeneity, state-dependent transcriptional changes, and intercellular communication networks. After stringent quality control, no substantial batch effects were observed. We identified five major T-cell subsets, with natural killer T (NKT) cells representing the most abundant population. Notably, naïve T cells and T helper 2 (Th2) cells were detected exclusively in active EoE samples, whereas regulatory T (Treg) and Th17 cells were present in all groups. The abundance of Tregs surpassed that of Th17 cells in active EoE but was similar to Th17 levels in normal and remission tissues. Functional enrichment analysis revealed a preferential association of NKT cells with receptor-binding functions. Th2 and naïve T cells shared signatures related to ribosome biology; naïve T cells additionally exhibited 5'-UTR binding and translation-regulator activity, aligning with their maturation potential. Consistent with the non-malignant nature of EoE, copy-number variation signals were minimal. Cell-type-specific differential expression analysis uncovered activated immune programs in NKT cells from active EoE, enriched for cytokine activity, along with epigenetic and transcriptional alterations in Tregs, including demethylase-linked functions, and protein-folding-related changes in Th17 cells. Cell-cell communication inference indicated a substantial rewiring of interaction networks in active EoE, suggesting activation of IL-16, IL-10, TRAIL, and PECAM1 pathways and heightened outgoing signaling from Th2 cells. Across all conditions, NKT cells served as dominant signaling senders and receivers. Collectively, these results delineate the T-cell composition and signaling circuits specific to active EoE, offering mechanistic insights into the maintenance of disease activity. - Source: PubMed
Publication date: 2026/08/27
Cui JiangheYu LongmeiWang RuiGui Yifang - - Source: PubMed
Efremov Dimitar G