Human CXCL9 MIG Elisa kit
- Known as:
- Human CXCL9 MIG Elisa reagent
- Catalog number:
- BEK1035
- Product Quantity:
- 96 T
- Category:
- Elisa Kits
- Supplier:
- Biospes
- Gene target:
- Human CXCL9 MIG Elisa kit
Related genes to: Human CXCL9 MIG Elisa kit
- Gene:
- CXCL9 NIH gene
- Name:
- C-X-C motif chemokine ligand 9
- Previous symbol:
- CMK, MIG
- Synonyms:
- SCYB9, Humig, crg-10
- Chromosome:
- 4q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-05-28
- Date modifiied:
- 2016-10-05
Related products to: Human CXCL9 MIG Elisa kit
Related articles to: Human CXCL9 MIG Elisa kit
- Neuroinflammation and systemic immune dysregulation are increasingly recognized as key contributors to secondary brain injury after aneurysmal subarachnoid hemorrhage (aSAH). However, the temporal relationship between circulating cytokine responses and innate-like lymphocyte populations, particularly mucosal-associated invariant T (MAIT) cells, remains poorly characterized. - Source: PubMed
Publication date: 2026/08/20
Merei AkosBalazs NoemiChayeen Brotzki Da CostaEngelmann PeterBerki TimeaErdő-Bonyár SzabinaSimon DianaMolnar TihamerOlah CsabaCsecsei Peter - Few large-scale population-based studies have examined the association between COVID-19 and respiratory aspergillosis. Using nationwide data, we investigated whether SARS-CoV-2 infection increases respiratory aspergillosis incidence and whether COVID-19-associated aspergillosis affects COVID-19 severity. We also analyzed public COVID-19 transcriptomic datasets to assess effects on airway structural and immune cells. - Source: PubMed
Publication date: 2026/09/03
Kim Jong SeungPark Jun HyungKim JuhyunLee Yong ChulYang Ji WonYou Yeon SeokKim GwangsuKim WankyuJeong Jae Seok - Immune checkpoint inhibitor-mediated pneumonitis (CIP) constitutes a major toxicity that limits the clinical application of cancer immunotherapy, whereas its underlying mechanisms remain incompletely understood. Current management relies on nonspecific immunosuppressants, lacking precision therapies. Although single-cell RNA sequencing (scRNA-seq) of bronchoalveolar lavage fluid (BALF) has implicated T cell activation and inflammatory myeloid responses in CIP pathogenesis, critical gaps persist regarding interstitial lung immunity and mechanisms governing monocyte/macrophage-T cell co-enrichment and crosstalk. We aimed to delineate the lung immune circuits that drive CIP and to identify targetable monocyte/macrophage-T cell pathways that could be leveraged for precision intervention. To elucidate CIP pathogenesis, we performed integrated scRNA-seq analysis of BALF from CIP and CIP patients with validation in a prospective cohort using flow cytometry, enzyme-linked immunosorbent assay, Western blotting, and quantitative polymerase chain reaction. Mechanistic studies were performed using an established tumor-bearing forkhead box P3-diphtheria toxin receptor-green fluorescent protein () mouse model of programmed death-1 inhibitor-induced CIP via micro-computed tomography, histopathology, scRNA-seq, flow cytometry, multiplex immunofluorescence, Western blotting, Transwell migration assays, and pharmacologic interventions. In CIP patient BALF and mouse lung tissues, CD8 T cells expressing cytotoxic effectors and C-X-C chemokine receptor 3 (CXCR3) expanded concomitantly with distinct C-C chemokine receptor 2 (CCR2) monocyte-derived macrophages (MoMΦ) exhibiting a highly inflammatory phenotype, while tissue-resident macrophages were markedly reduced. Mouse models revealed that expanded CCR2 MoMΦ originating from circulation replenished the depleted niche of lung-resident interstitial macrophages. Mechanistically, integrated in silico prediction and experimental validation demonstrated that CCR2 MoMΦ recruited CD8 T cells via the C-X-C motif chemokine ligand 9/10 (CXCL9/10)-CXCR3 axis. Conversely, CD8 T cells drove CCR2 MoMΦ expansion and pro-inflammatory phenotype via the interferon-γ (IFN-γ) axis, suggesting the existence of a positive feedback loop between these cell types. Pharmacological targeting of CCR2/CCR5 or CXCR3 signaling attenuated pneumonitis, reduced pulmonary CCR2 MoMΦ infiltration, diminished pathogenic T cell activation and cytotoxicity, and improved survival without compromising antitumor immunity. Our findings establish CCR2 MoMΦ and the IFN-γ-CXCL9/10-CXCR3 axis as core drivers of CIP pathogenesis and validate their therapeutic targeting potential. This work provides a scientific foundation for developing CIP-specific prevention and treatment strategies. - Source: PubMed
Publication date: 2026/09/02
Cui XiaoranZhi RenyongLi XiaoyanJi YinmingHu ZhisongCui PengfeiQin YuhuiLi TaoWu LiangliangWang LingxiongLi JinfengBai YibingLi HuiLiu TianyiHu Yi - Triple-negative breast cancer (TNBC) shows marked intratumoral heterogeneity and variable responses to neoadjuvant chemotherapy (NAC), but the cellular determinants of treatment response remain incompletely defined. - Source: PubMed
Publication date: 2026/08/19
Gao MenglongLiu ZhenXi LiliDuan HongliangGuo Jingjing - Cancer immunophenotypes-immune desert (ID), immune excluded (IE), and immune inflamed (II)-reflect intratumoral immune activity and correlate with immunotherapy efficacy. Serological methods for non-invasive immunophenotyping would be clinically valuable for selecting therapies. We measured plasma concentrations of cytokines (IL-6, IL-10, IL-16, IL-18, VEGF), chemokines (CXCL9, CXCL13), and soluble membrane molecules (sPD-1, sPD-L1, sCTLA-4, sCD163) in 49 patients with head and neck squamous cell carcinoma (HNSCC) and 22 healthy donors using an automated chemiluminescence enzyme immunoassay system. Plasma levels of IL-6, IL-10, VEGF, CXCL9, CXCL13, and sCD163 were significantly higher in patients with HNSCC than in healthy donors. IL-10 levels trended higher in the order ID > IE > II, whereas CXCL9, CXCL13, and sCD163 levels trended higher in the order II > IE > ID. This progressive trend across phenotypes was further enhanced by calculating the ratios of these markers to IL-10. Significantly higher sPD-1 levels were observed in the II phenotype. These results indicate that plasma concentrations and ratios of CXCL9, CXCL13, sCD163, IL-10, and sPD-1 serve as potential surrogate biomarkers reflecting tumor immunophenotypes in HNSCC. - Source: PubMed
Publication date: 2026/09/02
Suzuki SusumuIto HideakiOkubo IkukoUga HitoshiIwanaga NiinaHasegawa TakehiroNakamura HiromuInukai DaisukeSano RuiTakahara TaishiTsuzuki ToyonoriOgawa Tetsuya