Cymax Human MCP-1 ELISA Kit
- Known as:
- Cymax Human MCP-1 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- lf-ek0265
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- Cymax Human MCP-1 ELISA Kit
Related genes to: Cymax Human MCP-1 ELISA Kit
- Gene:
- CCL2 NIH gene
- Name:
- C-C motif chemokine ligand 2
- Previous symbol:
- SCYA2
- Synonyms:
- MCP1, MCP-1, MCAF, SMC-CF, GDCF-2, HC11, MGC9434
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-05
- Date modifiied:
- 2016-10-05
- Gene:
- SLC25A14 NIH gene
- Name:
- solute carrier family 25 member 14
- Previous symbol:
- -
- Synonyms:
- BMCP1, UCP5
- Chromosome:
- Xq26.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-09
- Date modifiied:
- 2016-10-05
Related products to: Cymax Human MCP-1 ELISA Kit
Related articles to: Cymax Human MCP-1 ELISA Kit
- The mechanisms that cause hypertension remain elusive despite more than a century of investigation. Some of its triggers include aging, sex, salt, diet, stress, experience with adversity, socio-cultural-economic disparities, and poor-quality sleep. The renin-angiotensin-aldosterone and the endothelin systems and other hormones contribute to varying degrees to the rise in BP and target organ damage. It has become increasingly recognized that inflammation and the innate and adaptive immune systems play a role in the etiopathogenesis of hypertension. We review here the participation of different cellular and molecular (genetic and epigenetic) mechanisms that play a role in hypertension via the immune system, including neutrophil extracellular traps, memory T cells, and aldosterone-modulated trained immunity mediated by monocytes/macrophages. Molecular mechanisms, including the effects of neutrophil gelatinase-associated lipocalin as an immunomodulator, and the role of isolevoglandins in mediating oxidative stress-induced activation of the adaptive immune system are analysed. We conclude by summarizing potential therapeutic avenues to address inflammation in hypertension. - Source: PubMed
Publication date: 2026/09/18
Fields EviatarBerillo OlgaSchiffrin Ernesto L - pneumonia triggers a complex, dynamic host response, yet the cellular coordination of inflammation and repair remains poorly defined. - Source: PubMed
Publication date: 2026/09/08
Zong FuliangWang YanHu LingfeiLi LuZhou DongshengZhao JinYang Huiying - Hepatocellular carcinoma (HCC) commonly develops in the context of chronic liver injury and fibrosis, and its immune evasion and therapeutic resistance are shaped not only by tumor-intrinsic factors but also by persistent interactions between the tumor stroma and immune cells. Hepatic stellate cells (HSCs) represent an important source of cancer-associated fibroblasts (CAFs) in HCC. HSC-derived CAFs can restrict the infiltration and function of effector T cells and promote the accumulation of immunosuppressive cells through CAF-associated and multicellular signaling networks, including TGF-β/SMAD, IL-6/STAT3, CXCL12/CXCR4, and CCL2/CCR2, as well as through extracellular matrix remodeling, vascular abnormalities, hypoxia, and metabolic reprogramming. Importantly, mediators such as IL-6 and CCL2 are not specific to HSC-derived CAFs and can also be produced by immune cells, hepatocytes, and other cellular populations within the HCC microenvironment. Conversely, cytokines released by distinct T-cell subsets, including IL-17A, TGF-β, IL-10, IFN-γ, and TNF-α, can in turn shape CAF activation, inflammatory states, and matrix-remodeling programs, thereby establishing a dynamic immune-stromal feedback loop. Focusing on the heterogeneity of CAFs and T cells, this review systematically summarizes the major mechanisms underlying bidirectional crosstalk between HSC-derived CAFs and T cells and their stage-specific roles in chronic liver injury, HCC initiation, progression, and therapeutic resistance. We further discuss potential therapeutic strategies involving CAF modulation, stromal remodeling, combination immunotherapy, and patient stratification. Current evidence suggests that this crosstalk axis may provide an important framework for understanding immune exclusion and therapeutic resistance in HCC. However, its clinical translation remains constrained by CAF heterogeneity, limited targeting specificity, insufficient causal evidence in humans, and safety concerns in the setting of underlying liver disease. - Source: PubMed
Publication date: 2026/09/07
Pan KechuanMa Chunlian - Conventional fractionated radiotherapy (CFRT) remains a mainstay for many solid tumors, yet it often fails to elicit durable anti-tumor immunity. How CFRT engages tumor-cell programs to shape the immune microenvironment and determine therapeutic outcome remains unclear. Here we show in preclinical mouse models that CFRT is associated with increased tumor-cell HMGB1 relative to stereotactic body radiotherapy (SBRT), and that loss of tumor-cell HMGB1 eliminates the efficacy gap between the regimens. HMGB1 deficiency markedly restrains tumor progression under CFRT in immunocompetent, but not immunodeficient, hosts, accompanied by increased intratumoral CD8 T cells and effector function. In esophageal squamous cell carcinoma (ESCC) specimens from patients receiving CFRT plus platinum-based chemotherapy, tumor-cell HMGB1 increases after treatment, and elevated pretreatment HMGB1 is associated with poor treatment response, reduced post-treatment CD8 T-cell infiltration, and adverse outcomes. Mechanistically, HMGB1 restrains CFRT-induced CD8 T-cell immunity through two convergent arms: CCL2-CCR2-dependent accumulation of suppressive monocytes and FUT8-linked regulation of PD-L1 fucosylation in tumor cells. TCF4 is linked to HMGB1-dependent induction of CCL2 and FUT8. Blocking CCL2 or inhibiting PD-L1 fucosylation restores CD8 T-cell effector function and enhances CFRT efficacy, alone or in combination with anti-PD-1 therapy. Together, these findings identify a tumor-cell HMGB1 program that underpins CFRT-associated immune suppression and nominate actionable targets to improve CFRT-immunotherapy combinations. - Source: PubMed
Publication date: 2026/09/19
Chen ChenShi JiahongCao PeihaiBai JuanLei YutiantianHuang MengdiSi MingjunWang RuiyingLv TingtingJia RuiMu QiuyuJiang DinggeHou YuzhuHuang Shan - Hyperammonemic rats show neuroinflammation and enhanced GABAergic neurotransmission in cerebellum. Treating hyperammonemic rats with compounds that reduce GABA receptors activation reduces some aspects of neuroinflammation. How GABAergic neurotransmission affects glial activation and the mechanisms involved are not clear. We hypothesized that, in cerebellum of hyperammonemic rats, enhanced GABA receptors activation contributes to activation of microglia, which releases pro-inflammatory factors that activate astrocytes, and that blocking GABA receptors with bicuculline will reverse these effects. The first aim was to characterize the effects of reducing GABA receptors activation with bicuculline in cerebellum of hyperammonemic rats on microglia and astrocytes activation. Neuroinflammation enhances GABAergic neurotransmission in cerebellum of hyperammonemic rats by activating the TNFα-TNFR1-S1PR2-CCl2-CCR2-BDNF-TrkB pathway and the TNFα-TNFR1-NFkB-glutaminase-GAT3 pathway. The second aim of this work was to assess if GABA receptors over-activation contributes to enhance activation of these pathways by analyzing if it is reversed by bicuculline. Hyperammonemia induces pro-inflammatory microglia activation, increasing NFκB, MAPK p38, STAT3, TNFα and glutaminase in microglia and TNFα, IL-1α and C1q which induce astrocytes activation. Enhanced GABA receptors activation also contributes to activate the TNFα-TNFR1-S1PR2-CCl2-CCR2-BDNF-TrkB, and TNFα-TNFR1-NFkB-glutaminase-GAT3 pathways. All these effects are reversed in cerebellar slices from hyperammonemic rats by blocking GABA receptors with bicuculline, indicating that are triggered by GABA receptors over-activation. These data support that enhanced GABA receptors activation in cerebellum induces pro-inflammatory effects in hyperammonemic rats and anti-inflammatory effects in control rats. - Source: PubMed
Publication date: 2026/09/19
Palomares-Rodriguez AndreaArenas Yaiza MFelipo Vicente