Mouse CXCL16 ELISA kit
- Known as:
- Mouse CXCL16 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- BEK1038
- Product Quantity:
- 96 T
- Category:
- Elisa Kits
- Supplier:
- Biospect
- Gene target:
- Mouse CXCL16 ELISA kit
Related genes to: Mouse CXCL16 ELISA kit
- Gene:
- CXCL16 NIH gene
- Name:
- C-X-C motif chemokine ligand 16
- Previous symbol:
- -
- Synonyms:
- SR-PSOX, CXCLG16, SRPSOX
- Chromosome:
- 17p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-21
- Date modifiied:
- 2016-10-05
Related products to: Mouse CXCL16 ELISA kit
Related articles to: Mouse CXCL16 ELISA kit
- Asthma is a chronic inflammatory airway disease characterized by Th2- dominant immune responses, airway hyperresponsiveness, and structural remodeling. Although inhaled corticosteroids and biologics are effective for many patients, a substantial proportion remains poorly controlled and experiences treatment-related adverse effects. Probiotics have emerged as immunomodulatory agents in asthma, but existing studies predominantly focus on oral administration and gut-lung axis regulation. Whether direct respiratory administration of probiotics can modulate the pulmonary immune microenvironment and alleviate asthma remains largely unexplored. - Source: PubMed
Publication date: 2026/09/01
Yang XinYu FanWu XiaochengLi ShuxianWang YingshuoHu ZhongXie YichengMa DaqingWu Lei - Vitiligo is an autoimmune disorder marked by melanocyte destruction and epidermal depigmentation, primarily driven by inflammatory and oxidative stress within the affected skin lesions. Consequently, there is an urgent need for therapeutic strategies focused on protecting melanocytes and replenishing melanin for effective vitiligo management. In this study, a novel microneedle-based therapeutic platform (C/D/E@MN) was fabricated that was composed of cuttlefish ink nanoparticles (CINPs) for melanin supplementation, dipotassium glycyrrhizinate (DPG) for inflammation regulation, and skin-derived exosomes (EXO) to promote melanocyte proliferation. In addition, microneedles with varying dissolution profiles (swellable, slow-dissolving, and fast-dissolving) were designed and evaluated their performance to optimize therapeutic efficacy. In vitro results demonstrated that fast-dissolving microneedles (FDMN) significantly reduced cellular reactive oxygen species (ROS) and the secretion of vitiligo-related inflammatory cytokines and chemokines, such as IL-8, CXCL-16, and HMGB-1. Upon a vitiligo mice model, C/D/E@FDMN treatment group generated a significant increase in skin melanin content and a 15.5% reduction of whitening degree. The microneedles protected melanocytes and promoted lesion repigmentation through synergistic antioxidant, anti-inflammatory and cyto-proliferative mechanisms, offering a promising strategy for improved vitiligo therapy. - Source: PubMed
Publication date: 2025/08/06
Li WeimiaoShi YanZhan RuiminLiu LuWang JiaruiLee MinhyeockZhang BingqiangLiang ShaoshuaiWang ZhiguoKong Ming - The tumor microenvironment is crucial for cancer progression, but the mechanisms underlying the tumor-immune cell interactions in it remain poorly understood. Here, we identified latent transforming growth factor-β (TGFβ) binding protein 4 (LTBP4) deficiency in colorectal cancer (CRC) as a critical driver that reprogrammed tumor-associated macrophages (TAMs) and induced a distinct subset, which promoted tumor progression by coordinating immune evasion and extracellular matrix (ECM) remodeling. Clinically, LTBP4 deficiency correlated with CRC progression and poor patient survival. knockout markedly promoted tumor growth and metastasis in immunocompetent mice, an effect attenuated in immunodeficient hosts, establishing the essential role of host immunity in mediating the effects of LTBP4 deficiency. Single-cell RNA sequencing revealed that LTBP4 deficiency induced a mannose receptor C-type 1-positive (MRC1)/CD44 TAM subset and correlated with reduced CD8 T cell infiltration. Mechanistically, LTBP4 deficiency increased active TGFβ1 levels, which acted in a paracrine manner to up-regulate MRC1 in TAMs, whereas autocrine signaling induced HAS2 (hyaluronan synthase 2) expression and hyaluronan production to increase CD44. CD44 signaling in TAMs up-regulated matrix metalloproteinases for collagen degradation, whereas MRC1 mediated collagen internalization, cooperatively remodeling the ECM to facilitate tumor invasion. The TGFβ1-driven MRC1/CD44 TAMs further suppressed CD8 T cell function by diminishing the C-X-C motif chemokine ligand 16-C-X-C motif chemokine receptor 6 (CXCL16-CXCR6) axis. Therapeutically, targeted depleting MRC1/CD44 TAMs enhanced the efficacy of PD-1 (programmed cell death-1) blockade in LTBP4-deficient tumors. Our study positions LTBP4 as a key modulator of tumor progression and reveals a therapeutic strategy for LTBP4-deficient CRC. - Source: PubMed
Publication date: 2026/08/26
Ji SongtaoDu ShuyaMiao GeYang XiaohuaWang HaojiaLi XuemeiMa WanqiWei DanCao TianyuZhou MingzhenYu JianingCheng XiangshuZhang YuanciHan HuaNie YongzhanLi JipengQin HongyanWang LiangWang XinLu YuanyuanZhao Xiaodi - Chemokines are traditionally known for their roles in immune cell recruitment during inflammation, but emerging evidence suggests that they may also directly regulate cellular states within the central nervous system. Specifically, it remains unclear whether CXCL16 affects microglial functional states in ischemic stroke. Here, we demonstrated that recombinant CXCL16 (rCXCL16) modulated the expression of inflammation- and repair-associated markers in primary microglia and in the ischemic brain. Functionally, microglia pretreated with rCXCL16 increased HT-22 cell viability and reduced apoptosis in an indirect co-culture system. Consistently, in vivo administration of rCXCL16 reduced infarct size, restored neurobehavior performance, and suppressed apoptosis in experimental stroke in mice. These findings identify rCXCL16 as a modulator of microglial responses and suggest that its neuroprotective effects are associated with reduced inflammatory marker expression and attenuation of apoptotic injury after ischemic stroke. - Source: PubMed
Publication date: 2026/08/22
Sun HongyiZhou ChengHu JingLuan TengfeiLu Taoli - Glioblastoma is among the most lethal human malignancies. Immune-based therapies have failed due to a strong immunosuppressive tumor microenvironment (TME). We uncovered that LAIR-1 expressed by tumor cells simultaneously drives TME fibrosis and inhibits migration of immune cells to brain tumors, thus achieving powerful immune exclusion. We demonstrate that glioma-cell-specific LAIR-1 knockdown (KD), but not LAIR-1 KD from host cells, significantly extends survival in an immune-dependent manner. Glioma-cell-specific LAIR-1 signals through SHP2 to activate JNK -which on one hand sustains high levels of Lysyl Oxidase-Like 1 and collagen I to block immune cells' entry- and on the other hand suppresses STAT3 signaling. In the absence of LAIR-1, gliomas' collagen-dense ECM becomes disassembled and, through STAT3-driven upregulation of ADAM10 and ADAM17, promotes release of CXCL16, and recruitment of NK cells and cytotoxic T cells. Combining LAIR-1 KD with immune-stimulatory gene therapy achieved 100% long-term survival with durable immunological memory in immunocompetent mice. Pharmacological SHP2 inhibition in LAIR-1 WT mouse and human glioma cells recapitulated the LAIR-1 KD molecular phenotype and similarly potentiated gene therapy. These findings define LAIR-1 as a tumor-cell-intrinsic pro-fibrotic and immunosuppressive checkpoint and identify the LAIR-1>SHP2>JNK>CXCL16 and/or LOXL1 axis as a therapeutic target for sensitizing glioma to immunotherapy. - Source: PubMed
Publication date: 2026/08/05
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