IL16 Antibody
- Known as:
- IL16 Antibody
- Catalog number:
- XW-7288
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- IL16 Antibody
Related genes to: IL16 Antibody
- 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: IL16 Antibody
Related articles to: IL16 Antibody
- Diabetic retinopathy (DR) requires robust biomarkers. To overcome the limitations of bulk sequencing, we integrated single-cell eQTL mapping with Mendelian randomization to identify causal cell populations and genes. CD8 Teff cells were expanded in peripheral blood, showing elevation in non-DR diabetes and reaching maximal levels in DR. Mendelian randomization analysis implicated IL2RB as a putative causal marker, with the lead eQTL SNP rs3184504 demonstrating strong association ( = 8.5467 × 10). Colocalization analysis with DR GWAS and validation in bulk data reinforced this signal. In tissues, CellChat predicted more interactions for IL2RB compared to IL2RB CD8 Teff cells, including IL16-CD4 with macrophages and NAMPT interactions with both ITGA5+ITGB1 and INSR on endothelial cells, implicating immune-vascular regulation. Together, these findings nominate IL2RB as a biomarker and therapeutic target while clarifying mechanisms underlying DR. - Source: PubMed
Publication date: 2026/08/05
Cao LizhiWang ZumingCai XiaoweiZhou YongkangYan Yu - To investigate a novel regulatory pathway mediated by exosomal non-coding RNA in rats with spinal cord injury (SCI). - Source: PubMed
Yin NaWu XiaolongXie YanZhou YingjieZhuo HanjieWang QingfengHuang Yong - Vitiligo is a multifactorial melanocyte disease caused by immune-mediated destruction. Inflammatory cytokines are central to vitiligo pathogenesis. Interleukin-16 (IL-16) is a pro-inflammatory cytokine implicated in the recruitment and activation of T-cells (CD4+), indicating that it may play a role in autoimmune inflammation. Nevertheless, the IL-16 expression and its genetic variants in vitiligo are poorly understood. This study involved 100 patients diagnosed with vitiligo and 50 age and gender harmonized controls. TaqMan assays were used to genotype the rs4072111 polymorphism, and qRT-PCR was employed to determine the IL-16 relative expression. VIDA and VASI scores were used to assess clinical activity and severity. Patients had a higher prevalence of C/T, T/T genotypes, and T allele than controls. IL-16 expression was notably higher in patients. The increased level of relative expression was associated with active disease. This study indicates that IL-16 rs4072111 polymorphism and increased IL-16 gene expression were significantly associated with vitiligo. Higher IL-16 expression was also linked to greater disease activity. These findings emphasize that IL-16 may serve as a promising biomarker for disease susceptibility and activity, although further validation in larger and more diverse populations is required. - Source: PubMed
Publication date: 2026/07/30
El Derbaly Sara AMabrouk Abd-Allah Ahmed EmanGaber Antar Farag AzzaEl-Kousy Salah MEl Sayed Ibrahim El Tantawy - : Extracranial arteriovenous malformations (eAVMs) are aggressive vascular anomalies consisting of abnormal blood vessels (BVs) and multiple other cell types, including macrophages. Although inflammation and the presence of immune cells are characteristics of eAVMs, the contribution of macrophage polarization to eAVM pathophysiology is unknown. : In this study, pediatric eAVM tissues and adjacent control tissues were analyzed using immunohistochemistry (IHC) and immunofluorescence (IF) to assess M1 and M2 macrophage localization, loss of endothelial CD31 expression, and expression of the immune-regulatory protein PDL-1. In addition, serum samples from eAVM patients were analyzed using a human inflammation antibody array to profile cytokines and other circulating factors associated with M2 macrophage and immunosuppressive microenvironment. : eAVM tissues demonstrate accumulation of M2-polarized macrophages around abnormal CD31 BVs, while M1 macrophages were primarily associated with normal appearing CD31 vessels. eAVM tissues demonstrated increased expression of PD-L1 in regions enriched with M2 macrophages, which were absent in paired control tissues. Serum analysis revealed increased levels of circulating factors associated with M2 macrophages and immune suppression, including PDGF-BB, IL-4, and IL-16. : These findings suggest that CD31 vessels in eAVMs are associated with enrichment of M2 macrophages and a microenvironment suggestive of localized immune regulation. These observations are hypothesis-generating and warrant validation in larger patient cohorts and future mechanistic studies. - Source: PubMed
Publication date: 2026/07/07
Mehdi Syed JBauer Michael AZhang HaihongSun Ravi WBowen JordanMatre Stetson VanRichter Gresham TStrub Graham M - Molting is an essential physiological process for crustaceans and is accompanied by dynamic immune fluctuations. 20-Hydroxyecdysone (20E), a key steroid hormone that drives the molting process, rises sharply at the pre-molt stage. However, the molecular mechanisms by which 20E coordinates stage-dependent immune regulation remain poorly understood. In this study, a JUN homolog was identified from Eriocheir sinensis and designated as EsJUN. Sequence analysis showed that EsJUN contains a conserved bZIP/BRLZ domain, and molecular docking predicted a potential binding mode between EsJUN and EsERK. Further analyses showed that both the mRNA expression and phosphorylation levels of JUN and ERK were significantly higher at pre-molt stage than those at post-molt stage. Moreover, exogenous 20E injection significantly enhanced ERK and JUN phosphorylation, promoted the nuclear translocation of JUN, and was associated with enhanced ERK-JUN co-association. In parallel, the inflammation-related genes IL-16, LITAF and ILF were also significantly upregulated at the pre-molt stage. Functional analyses showed that EsJUN knockdown significantly reduced the expression of these inflammatory genes. Consistently, ERK inhibition produced a similar suppressive effect on inflammatory transcription and also decreased EsJUN expression, phosphorylation as well as nuclear accumulation. Collectively, these findings suggest that EsJUN contributes to the expression of inflammation-related genes during molting in E. sinensis, providing new insight into the molecular linkage between endocrine signaling and immune regulation in crustaceans. - Source: PubMed
Publication date: 2026/07/25
Xi YutingYu JinmingXu YiyangLiu ChangTu YuhanMa YuhanLi SiyueGuo JunweiYang DazuoYi QilinHuang Shu