Anti_Mouse, mab CXCL16 Source Rat
- Known as:
- Anti_Mouse, mab CXCL16 Source Rat
- Catalog number:
- 103-M359
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Mouse mab CXCL16 Source Rat
Related genes to: Anti_Mouse, mab CXCL16 Source Rat
- 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: Anti_Mouse, mab CXCL16 Source Rat
Related articles to: Anti_Mouse, mab CXCL16 Source Rat
- Persistent HPV infection is a major risk factor for cervical cancer, but the immune mechanisms behind HPV-induced tumor progression are not fully understood. Neutrophils may play a key role in immune remodeling and evasion within the HPV-infected tumor microenvironment. We integrated 31 cervical samples (including HPV-infected and non-infected normal, tumor, and HSIL tissues) to construct a single-cell atlas of 141,785 cells. Neutrophil heterogeneity, cell-cell communication, and immunosuppressive programs were systematically analyzed. Transcriptomic findings were validated via immunohistochemistry, immunofluorescence, and Mendelian randomization (MR). HPV infection dramatically remodeled the immune landscape, inducing robust neutrophil and plasma cell infiltration while reducing T cell abundance. Neutrophils in HPV+ tissues were terminally differentiated and displayed a distinct CXCL8 phenotype. These CXCL8 neutrophils were identified as late-stage, transcriptionally defined low-plasticity state enriched with immunosuppressive genes (e.g., SPP1, VEGFA). They exhibited enhanced interactions with T cell subsets, particularly regulatory and cytotoxic T cells, via ligands like CXCL16 and APOE, suggesting direct immunosuppressive crosstalk. MR analysis indicated a causal role for CXCL8 in cervical cancer, and spatial protein assays confirmed elevated CXCL8 and its receptor CSF3R in HPV+ tumors. HPV infection expands immunosuppressive CXCL8 neutrophils that modulate T cell activity and promote immune escape. CXCL8 is identified as a causal factor and potential therapeutic target in HPV-driven cervical cancer. - Source: PubMed
Liu MiaomiaoZhang LinaFan YananHan LinaTian LeiPeng LiliHe LiyaLi QiaofangYan XiaoluShen Ting - Methotrexate (MTX) is a widely used chemotherapeutic and immunosuppressive agent; however, one of clinical limitations of its use is renal toxicity. CXCL16 is a transmembrane chemokine that can be cleaved by ADAM family proteases, particularly ADAM10, to generate a soluble form that acts as a chemoattractant for CXCR6-expressing cells such as T lymphocytes. This process may contribute to inflammatory renal injury. This study investigated the role of CXCL16/ADAM10 in MTX-induced nephrotoxicity and assessed the renoprotective effects of simvastatin (SIM). Fifty male Wistar rats were randomly assigned to five groups: control, SIM (40 mg/kg), MTX (20 mg/kg) and two combination groups receiving MTX with SIM (10 or 40 mg /kg). SIM was administered orally for 10 days, while MTX was administered as a single i.p. dose on day 4. Hematological parameters, markers of renal function, and renal histopathology were assessed. In addition, the expression of CXCL16, ADAM10, CD3, and fibrinogen was evaluated. MTX administration significantly elevated renal function markers compared with the control and SIM groups. Histopathological analysis revealed glomerular atrophy and mononuclear inflammatory cell infiltration in MTX-treated rats. Moreover, MTX markedly increased the expression of CXCL16, ADAM10, CD3, and fibrinogen in the glomeruli and tubulointerstitial regions. Treatment with SIM significantly improved renal function markers, attenuated histopathological damage, and reduced the expression of these inflammatory and injury-related proteins. CXCL16 and its processing enzyme ADAM10 play important roles in MTX-induced renal toxicity. SIM demonstrated a dose-dependent protective effect against MTX-induced renal injury, likely through modulation of inflammatory pathways involving CXCL16/ADAM10 signaling. - Source: PubMed
Publication date: 2026/07/02
Alradhi AluluAlelowi Abdulrahman AAlhowail Ahmad HAldubayan Maha AAbdel-Bakky Mohamed S - Parkinson's disease (PD) is a progressive neurodegenerative disorder with limited disease-modifying therapies. PANoptosis, an integrated form of programmed cell death involving apoptosis, pyroptosis, and necroptosis, has been implicated in neuroinflammation-related neurodegeneration. However, the roles of PANoptosis-related genes in PD remain unclear. - Source: PubMed
Publication date: 2026/06/30
Li ZhouYang RongFeng HaoSun MouLiu Hongjun - In brain tumors, the immunosuppressive microenvironment leads to tumor aggressiveness and immunotherapy resistance. To identify factors that regulate the glioma immune landscape, we took advantage of the disease trajectory of the MAPK-driven glioma, pleomorphic xanthoastrocytoma (PXA), which evolves from an immune-rich low-grade tumor to an aggressive glioma. - Source: PubMed
Publication date: 2026/06/30
Hashemi ElahehAkshaya Ravishkumar LakshmiWang LinBergland SpencerPiyadasa HadeeshaRanek Jolene SVoong VivaKshirsagar AdityaShai AnnyOberlton BenjaminKumar AnupamBerger Mitchel SChang Edward FOldham Michael CPrins Robert MBendall Sean CAngelo MichaelHervey-Jumper Shawn LOkada HidehoDiaz AaronPhillips Joanna J - Incomplete thermal ablation (iTA) for hepatocellular carcinoma (HCC) fosters an immunosuppressive microenvironment driving local recurrence, yet the metabolic cues linking tissue injury to immune evasion remain undefined. Bile acids, particularly lithocholic acid (LCA), are elevated post-ablation, but their functional role in HCC recurrence is unknown. Here, we investigate whether LCA accumulation after iTA promotes tumor recurrence by suppressing antitumor immunity and identify the underlying molecular mechanism. - Source: PubMed
Publication date: 2026/06/28
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