Mouse MDC _ CCL22 ELISA kit
- Known as:
- Mouse MDC _ CCL22 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- BEK1149
- Product Quantity:
- 96 T
- Category:
- Elisa Kits
- Supplier:
- Biospect
- Gene target:
- Mouse MDC _ CCL22 ELISA kit
Related genes to: Mouse MDC _ CCL22 ELISA kit
- Gene:
- CCL22 NIH gene
- Name:
- C-C motif chemokine ligand 22
- Previous symbol:
- SCYA22
- Synonyms:
- MDC, STCP-1, ABCD-1, DC/B-CK, A-152E5.1, MGC34554
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-22
- Date modifiied:
- 2016-10-05
Related products to: Mouse MDC _ CCL22 ELISA kit
Related articles to: Mouse MDC _ CCL22 ELISA kit
- Advanced cervical cancer has a poor prognosis due to chemoresistance and immunosuppression, while the prognostic value of chemokines-related genes (CRGs) remains underexplored. This study aimed to develop a prognostic signature based on CRGs and explore its clinical utility in cervical cancer risk stratification, microenvironment characterization, and therapeutic response prediction. - Source: PubMed
Publication date: 2025/10/28
Xu BingShi XinyanLiu YanfeiXu LyupingZhou Qingxue - Natural killer large granular lymphocytic leukemia (NK-LGLL) is a rare lymphoproliferative disorder lacking definitive clonality markers, complicating diagnosis and distinction from reactive NK-cell expansions. We previously proposed an NK-clonality score with high diagnostic accuracy, but a subset of patients remained unclassified. In this multicenter international study, we refined and validated updated diagnostic criteria using independent training (n=78) and validation (n=57) cohorts from three national registries (USA, Italy, France). The revised framework integrates NK-score parameters with CCL22 mutations and bone marrow biopsy (BMB) findings. Four major criteria were defined: NK-cell count ≥1.0×10⁹/L, KIR restriction, CD94/NKG2A overexpression, and somatic mutations in STAT3, TET2, or CCL22, the latter newly introduced. In the training cohort, 50 patients were classified as NK-LGLL by NK-score >4, 18 had intermediate scores (2-3), and 10 were diagnosed as reactive proliferations. CCL22 mutations were identified in 16 patients (20%), including 5 with intermediate scores who were reclassified as NK-LGLL; BMB supported the diagnosis in 2 additional cases, resulting in 57 NK-LGLL overall. These patients exhibited more cytopenias, higher treatment needs, and greater transfusion requirements compared to patients with alternative diagnoses. In the validation cohort (25 NK-LGLL and 32 reactive cases), CCL22 mutations were detected in 5 NK-LGLL (20%). Altogether, incorporation of CCL22 mutations reduced the fraction of unclassified patients, improved diagnostic sensitivity without compromising specificity, and may decrease reliance on invasive procedures. These revised international criteria represent a step toward standardized, molecularly guided NK-LGLL diagnosis. - Source: PubMed
Publication date: 2025/11/05
Pastoret CedricYang JunFeith David JRoussel MikaelMoignet AlineDighe ShubhaSolga Micheal DimitriMarchand TonyVisser GaranceGasparini Vanessa RebeccaTeramo AntonellaZambello RenatoLoughran Thomas PLamy Thierry - Neuroinflammation is recognized as a core pathogenic mechanism of postoperative cognitive dysfunction (POCD), with microglia hyperactivation and subsequent M1/M2 polarization imbalance identified as critical contributing factors. High-mobility group box 1 (HMGB1), a damage-associated molecular pattern (DAMP), amplifies neuroinflammation; however, whether it mediates POCD through regulating microglia polarization remains unclear. - Source: PubMed
Publication date: 2025/11/02
Zhao LiHuang QiLi NaLin WanCui XiangYang FanMa LinZhang HuiwenMa Hanxiang - Immunosuppression within the tumor microenvironment (TME) profoundly inhibits anti-tumor immunity, presenting a formidable challenge in cancer therapeutics. Despite this recognized obstacle, multi-targeted immunomodulatory strategies remain elusive. Here we developed a novel mRNA-lipid nanoparticle (LNP) vaccine designed to reprogram key cellular mediators of immune suppression within the TME, including C-C motif chemokine ligand 22 (CCL22), transforming growth factor-β (TGF-β), cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), Galectin-3, programmed cell death ligand 1 (PD-L1), indoleamine 2,3-dioxygenase 1 (IDO1), and arginase 1 (ARG1). This immunomodulatory vaccine was evaluated in a cohort of canines with spontaneous neoplasms, encompassing adrenal, hepatic, perianal, vulvar, and pulmonary malignancies. The vaccine demonstrated good tolerability, with only mild adverse events (Grade 1 anorexia, chills, and fatigue) observed in 25% of subjects (2/8). Remarkably, 75% of treated animals (6/8) achieved stable disease, with the median progression-free interval not yet reached a median follow-up of 168 days post-treatment initiation. Two dogs experienced disease progression. The overall disease control rate was 75%. In addition, vaccine administration reversed hematological and biochemical abnormalities and alleviated paraneoplastic syndromes associated with these malignancies. These findings demonstrate that our mRNA-LNP vaccine effectively exerts anti-tumor effects across various cancer types, offering a promising strategy for enhancing anti-tumor immunity in both veterinary and human oncology. - Source: PubMed
Publication date: 2025/10/31
Han TiyunLiu GuilaiBao ChenyiZong JianFei CaiyiLi JingXu ShiMa QingboQian Yingjuan - Tumor Metabolic Behavior modulates the immunosuppressive microenvironment through multiple pathways, thereby compromising anti-tumor immune responses. To date, there have been limited studies assessing the role of metabolic plasticity or immunometabolism in the tumor microenvironment (TME) during metastasis. Notably, emerging evidence suggests the presence of an immunosuppressive niche in brain metastases. This research aims to delineate distinct metabolic signatures in brain metastatic, investigate the impact of tumor-associated glycolysis on the development of brain metastases in lung adenocarcinoma, and characterize the lactylation regulation in this immunosuppressive microenvironment. - Source: PubMed
Publication date: 2025/10/29
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