rHu MIP-1-alpha
- Known as:
- rHu MIP-1-a
- Catalog number:
- AK8250-0100
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Akro
- Gene target:
- rHu MIP-1-alpha
Related products to: rHu MIP-1-alpha
Related articles to: rHu MIP-1-alpha
- Cyanidin-3-O-galactoside(C3G) has a variety of biological activities. Pulmonary fibrosis (PF) is a fatal interstitial lung disease. To define its pathogenic networks, we performed transcriptomic sequencing of lung tissues from five mouse groups: WT_Control, WT_Model, WT_Model_C3G, Control_Ccl3-/-, Model_Ccl3-/-. Comprehensive assessment of immune infiltration, weighted gene co-expression network, and functional enrichment verified that PF is tightly linked to immune microenvironment dysregulation. Seven machine learning algorithms identified five core immune-related targets: Ccl3, Xcl1, Pyy, Il31ra, Ppbp. Subsequent analysis prioritized Ccl3 and Ppbp as the key core pathogenic genes. Molecular docking clarified their binding modes and key interaction sites with C3G. Histopathological and biochemical assessments showed that the WT_Model group exhibited elevated expressions of Ccl3 and Ppbp, accompanied by marked inflammatory infiltration and collagen deposition. C3G intervention significantly ameliorated these PF phenotypes. Ccl3 knockout improved survival and ameliorated fibrotic pathology. Interaction modeling and correlation analyses identified Slc2a3 as a key Ccl3 downstream target. WB and IHC validation revealed reduced expression of Ccl3, Slc2a3, and α-SMA proteins in Model_Ccl3-/- compared to WT_Model, which suggested Ccl3 may positively regulate the expression of Slc2a3. Through transcriptome and external metabolome verification, it was found that Slc2a3 can regulate PF through metabolic pathways. In conclusion, this study confirmed the potential role of C3G in regulating Ccl3-related inflammation and metabolic pathways in bleomycin-induced PF, which is expected to become a new strategy for targeted therapy of PF and provide a theoretical basis for the development of clinical treatment. - Source: PubMed
Publication date: 2026/07/31
Tang XianZhao MengLi FeiBao XiaochaoWang DongxuHe YujingGao JunZhang GuokunWei Jie - Immune checkpoint inhibitor (ICI) therapy is often associated with immune-related adverse events including inflammatory arthritis (ICI-IA). However, the mechanisms underlying ICI-IA, especially its recurrence, are not well understood. In this study, we sought to elucidate mechanisms of recurrent ICI-IA by analyzing longitudinal synovial fluid (SF) samples from patients with ICI-IA. SF samples were collected from six ICI-IA patients at the first and second occurrences of ICI-IA and analyzed with single-cell RNA sequencing (n=3), single-cell TCR sequencing (n=3), single-cell BCR sequencing (n=3), and flow cytometry (n=6). SF samples from cancer-naïve osteoarthritis patients (n=6) were used as negative controls. Analysis revealed that effector CD8+ T cells and PD-1hiCXCL13hiCD4+ T cells were enriched in the SF of ICI-IA patients. Ninety three percent and fifty percent of the top ten expanded clones of effector CD8+ T cells and PD-1hiCXCL13hiCD4+ T cells, respectively, were shared between the first and second ICI-IA flare. These top clones were characterized by the production of pro-inflammatory type 1 cytokines including IFN, TNF, and IL-21, especially in the second flare, suggesting immune memory responses to cognate antigen. Cell-cell communication analysis suggested that effector CD8+ T cells and PD-1hiCXCL13h CD4+ T cells interacted with each other and with myeloid cells and B cells through chemokines (CXCL9/10/11/13, CCL3) and cytokines (MIF, IL-2/7/15/21). Overall, longitudinal SF analysis from ICI-IA patients revealed the expansion of effector CD8+ T cells and PD-1hiCXCL13hiCD4+ T cells with type 1 cytokine signatures that potentially contribute to development or recurrence of ICI-IA. - Source: PubMed
Publication date: 2026/07/31
Keam SynatLi Yuanteng JeffChu YanshuoTayar Jean HLu HuifangWu MichaelAgarwal Sandeep KJain NitinMsaouel PavlosDiab AdiWang LinghuaHaymaker CaraNurieva RozaKim Sang T - In order to investigate the therapeutic mechanism of Jianpiyiqi Granule in juvenile myasthenia gravis (JMG) and find the immune-associated cytokines or signaling pathways targeted by this intervention. - Source: PubMed
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