Anti-Mouse CD11c FITC 500 ug
- Known as:
- Antibody toMouse CD11c fluorecein 500 ug
- Catalog number:
- 11-0114-85
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD11c FITC 500
Ask about this productRelated genes to: Anti-Mouse CD11c FITC 500 ug
- Gene:
- ITGAX NIH gene
- Name:
- integrin subunit alpha X
- Previous symbol:
- CD11C
- Synonyms:
- CD11c
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-15
- Date modifiied:
- 2015-12-15
Related products to: Anti-Mouse CD11c FITC 500 ug
Related articles to: Anti-Mouse CD11c FITC 500 ug
- In an earlier murine model of myocardial infarction (MI), we showed that CD8 cells and myeloid dendritic cells (mDCs) infiltrate the infarcted myocardium within the first week. However, in humans, the spatial interplay between CD8 T cells and dendritic cells in the spatial context of human myocardial infarction remains underexplored. In the present study, we applied spatial transcriptomics and functional assays to characterize immune-stromal dynamics in infarcted myocardium and peripheral blood. Spatial transcriptomics analysis of infarcted human myocardium at days 2 and 6 post-MI, combined with peripheral blood flow cytometry and EPC colony-forming assays, was performed. Cell composition, pathway enrichment, and cell-to-cell communication analyses were conducted to map immune-stromal cells' dynamics across time points. Spatial mapping identified dynamic shifts in immune, fibroblast, and endothelial populations, with fibroblasts and endothelial cells remaining abundant throughout. CD8 T cells accumulated in ischemic regions while their circulating levels declined. Gene Ontology and pathway analyses of CD8A transcripts revealed enrichment of proinflammatory and NF-κB survival programs. ITGAX/CD33/THBD APCs progressively increased within infarct zones, activating antigen-presentation and leukocyte chemotaxis pathways. Early (day 2) APC-endothelial crosstalk showed the strongest predicted recruitment signals for CD8 T cells, which diminished by day 6. Finally, EPC colony-forming capacity showed a tendency for reduction in MI patients and inversely correlated with coronary lesion burden, indicating impaired vascular repair potential. This integrative spatial and functional study demonstrates that APC-driven CD8 recruitment and EPC dysfunction are key features of human MI. Immune-endothelial niches facilitate early cytotoxic T-cell infiltration, while progenitor depletion limits vascular regeneration. These findings provide mechanistic insight into immune-vascular imbalance during infarct healing and highlight potential therapeutic targets to modulate inflammation and restore vascular repair. - Source: PubMed
Publication date: 2026/03/26
Salybekov Amankeldi AShaikalamova SaidaKinzhebay AimanWolfien MarkusAsahara Takayuki - Air pollution particles exacerbate allergic asthma and can enhance inflammatory responses to allergen exposure, but the cellular mechanisms involved remain incompletely defined. We examined how diesel exhaust particles (DEP) enhance house-dust-mite (HDM) inflammatory responses within the lung and characterised potential mechanisms that may contribute to enhanced type 2 (T2) inflammatory responses. - Source: PubMed
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Meldrum KirstyKosoko Ayokulehin MuseLeonard Martin Oliver - Neurological deficits following spinal surgery represent a severe complication, and thermal damage from high-speed drills is considered a potential cause, but the underlying pathophysiology remains poorly understood. Here, we aimed to develop and characterize a novel mouse model of thermal-induced spinal cord injury (TiSCI). Given that surgical drilling can generate temperatures of 90 °C, we created a TiSCI model by applying a controlled thermal exposure (90 °C for 1 min) to the exposed thoracic cord in mice. The TiSCI model induced significant and persistent hindlimb motor deficits, accompanied by marked demyelination and progressive collagen deposition at the lesion site. Transcriptomic analysis by RNA-sequencing revealed that this pathology was associated with a significant upregulation of pro-fibrotic genes, including Col1a1, Col1a2, Tgfβ1, and Acta2. Using Col1a2-EGFP transgenic mice, we identified a prominent fibrotic scar composed of Type I collagen-producing cells at the lesion site, evident by 7 and 14 days post-injury, which spatially overlapped with demyelinated regions devoid of axons. KEGG pathway analysis highlighted pathways related to extracellular matrix organization, phagocytosis, and fibroblast activation. Notably, Scarb3 and Actg2 were upregulated early, while Itgax and Fzd7 were induced later, implicating both immune cell responses and Wnt/β-catenin signaling in fibrotic scar progression. In conclusion, this study established an experimental platform for investigating TiSCI in mice, providing first direct evidence that a thermal insult causes persistent neurological deficits by inducing a robust fibrotic response. The resulting collagenous scar acts as a physical barrier to axonal connectivity, establishing the fibrotic process as a key therapeutic target. - Source: PubMed
Publication date: 2026/03/17
Mashima ArataYokota KazuyaKobayakawa KazuSaiwai HirokazuKitade KazukiKishikawa JunSugano MamiSasaguri ShintaroTarukado KiyoshiKawaguchi KenichiOno GentaroMaeda TakeshiNakashima Yasuharu - We sought to determine changes in the expression of immune response-related genes occurring in surgical necrotizing enterocolitis (NEC) tissues from infants with necrosis severity and survival status. - Source: PubMed
Publication date: 2026/03/24
Garg Parvesh MohanRiddick RobinZhang PengboShenberger JeffreyVarshney NehaSawaya DavidGarg Padma - The cafeteria diet (CAFD) model has been used to mimic the Western-style "junk food" eating pattern, inducing obesity in rodents. As the dietary composition varies across studies, we developed a CAFD model based on commonly consumed Brazilian ultra-processed foods to evaluate its effect on weight gain, metabolic parameters, and gene expression in C57BL/6 mice. - Source: PubMed
Publication date: 2026/03/20
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