CD200R1 ELISA kit
- Known as:
- CD200R1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CD200R1-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CD200R1 ELISA kit
Related genes to: CD200R1 ELISA kit
- Gene:
- CD200R1 NIH gene
- Name:
- CD200 receptor 1
- Previous symbol:
- MOX2R
- Synonyms:
- OX2R, HCRTR2, CD200R
- Chromosome:
- 3q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-12
- Date modifiied:
- 2016-10-05
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- ObjectiveChronic migraine (CM) is characterized by central sensitization (CS), in which microglial activation plays a key role. The neuron-glia communication axis CD200/CD200R1 is a critical immunomodulatory pathway. This study investigated whether and how CD200/CD200R1 signaling modulates CS in a CM model.MethodsA CM mouse model was established by repeated nitroglycerin (NTG) injections. Pain thresholds were assessed. Protein expression in the trigeminal nucleus caudalis (TNC) was analyzed. The role of STAT6 was examined using inhibitor AS1517499.ResultsNTG treatment induced sustained hyperalgesia and downregulated CD200 and CD200R1 expression in the TNC. Administration of the CD200R1 agonist CD200Fc reversed pain hypersensitivity, suppressed the overexpression of CGRP and c-Fos, and reduced pro-inflammatory cytokines. CD200Fc promoted STAT6 phosphorylation and increased expression of anti-inflammatory markers (Arg-1, YM-1, YM-2). Inhibition of STAT6 phosphorylation abolished the therapeutic effects of CD200Fc on pain biomarkers without altering CD200R1 expression.ConclusionOur findings demonstrate that enhancing the CD200/CD200R1 pathway alleviates central sensitization and pain hypersensitivity in CM, likely by promoting an anti-inflammatory microglial phenotype via STAT6 phosphorylation. The CD200/CD200R1/STAT6 axis represents a novel therapeutic target for chronic migraine. - Source: PubMed
Publication date: 2026/09/21
Li ZiChaoLi DanFan ZhenZhenCai HongBinGe ZhaoMing - CD200 and its receptor CD200R form a myeloid-centered immune checkpoint that normally restrains myeloid activation and limits tissue damage, but many solid tumors co-opt this pathway to suppress antitumor immunity. CD200-CD200R signaling is highly context-dependent, varying even among models of the same cancer type. In melanoma and breast carcinoma, it can either suppress protumor inflammation or promote tumor growth and metastasis depending on the model, whereas in neuroblastoma; glioblastoma and other central nervous system tumors; cutaneous and head and neck squamous cell carcinoma; colorectal cancer; and several endocrine, ovarian, and pancreatic cancers, it consistently suppresses macrophage, dendritic cell, natural killer cell, and CD8+ T-cell activation, impairs phagocytosis and antigen presentation, and drives immunosuppressive infiltration. Non-small cell lung cancer and renal cell carcinoma emerge as two additional, less-characterized but clinically important contexts warranting further investigation. CD200R1-CD200 has also recently been identified as a macrophage phagocytosis checkpoint that functions independently of CD47-SIRPα, placing it within the expanding family of innate immune checkpoints. Rather than treating CD200-CD200R as a universally protumorigenic target, we propose a context-dependent framework-incorporating tumor type, microenvironmental architecture, and dominant myeloid and lymphoid programs-to guide tumor-specific therapeutic strategies in solid cancers. - Source: PubMed
Publication date: 2026/09/18
Sahu Manas RanjanEzhil InemaiAkkanapally VenuKumar AmanLiu Jin-QingBasu Sujit - Radiotherapy elicits dual immunomodulatory effects in cancer, activating antitumor immunity while paradoxically inducing immunosuppression, which limits therapeutic efficacy. The molecular pathways mediating postradiation immune escape in hepatocellular carcinoma (HCC) remain poorly defined. Here, we elucidate a previously uncharacterized mechanism whereby radiotherapy drives the accumulation of CD200 tumor-associated macrophages (TAMs) that suppress eosinophil-mediated antitumor immunity in patients with HCC. Through single-cell RNA sequencing of postradiotherapy HCC specimens, we demonstrated that radiation-induced DNA damage activated the cytosolic DNA-sensing STING pathway in TAMs, triggering NF-κB-dependent CD200 upregulation independent of canonical type I interferon signaling. These radiation-induced CD200 TAMs exhibited an immunosuppressive phenotype and correlated with adverse clinical outcomes in HCC patients. Mechanistically, CD200 TAMs established an immunosuppressive axis by recruiting CCR1 eosinophils through CCL3-mediated chemotaxis, subsequently inhibiting their antitumor functions via CD200-CD200R engagement. This interaction comprehensively suppressed NF-κB activation in eosinophils, impaired their antigen-presenting capacity and Th2 cytokine secretion and abrogated their ability to support CD8 T-cell-mediated cytotoxicity. Therapeutic blockade of CD200R following radiotherapy restored eosinophil effector functions, promoted central memory T-cell formation, and significantly enhanced tumor control across multiple preclinical HCC models. Remarkably, CD200R antagonism sensitized PD-1-refractory "cold" tumors to radioimmunotherapy combinations, overcoming primary resistance. Our findings establish STING-driven CD200 TAM accumulation and subsequent eosinophil dysfunction as critical determinants of radioresistance, positioning CD200R blockade as a promising therapeutic strategy to potentiate radioimmunotherapy responses in patients with HCC. Graphical abstract of the study findings. Radiotherapy-induced STING signaling activation promotes the accumulation of CD200 TAMs. These CD200 TAMs facilitate the recruitment of eosinophils via the CCL3-CCR1 chemotaxis axis while simultaneously suppressing eosinophil-mediated antitumor activity through CD200-CD200R engagement (left panel). Targeted blockade of CD200R following radiotherapy unleashed the antitumor potential of eosinophils, leading to enhanced infiltration and effector function of CTLs (right panel). - Source: PubMed
Publication date: 2026/08/13
Li KunLi SiqiQiu DongboQiu XiushengYu HaoyuanXiong YiLiang WeiLiang ZhixingCheng ShuqunLi HuaQin YunfeiYang YangYe Linsen - Ulcerative colitis (UC) is a chronic inflammatory disorder characterized by dysregulated mucosal immunity and impaired epithelial barrier function. CD200R is an inhibitory immune receptor involved in immune homeostasis, but its cell-specific expression pattern and functional role in UC remain unclear. - Source: PubMed
Publication date: 2026/06/25
Liu XiaomingHu YangWang JinRuan QingChen YujieGuo XiaoyaPeng LeiKe XiquanGuo Zhiguo - Thrombosis remains a major cause of morbidity and mortality in patients with cancer. Existing risk models fail to reliably predict venous thromboembolism (VTE), underscoring the need for more accurate predictive models. In this study, we conducted a high-throughput proteomic analysis of 1105 plasma proteins in peripheral blood samples from patients with newly diagnosed lung or gastric cancer who were prospectively monitored for VTE development. Using a Bayesian probabilistic machine learning approach, we developed a predictive model incorporating 11 protein biomarkers and five clinical parameters (age, sex, history of VTE, body mass index, and hemoglobin), which outperformed the standardly used Khorana prediction score [ statistic 0.84 (0.79 to 0.90) as compared with 0.36 (0.27 to 0.45)]. Orthogonal validation in an external placebo cohort from a phase 3 trial confirmed the model's predictive power. Further investigation into the mechanistic role of CD200 receptor 1 (CD200R1), an immune checkpoint receptor known to limit leukocyte inflammatory response that contributed strongly to the model, showed that reduced concentrations in plasma correlated with higher D-dimer concentrations and thrombosis risk. CD200R1-deficient mice were characterized by features of a prothrombotic state, with elevated thrombin-antithrombin complexes, increased interleukin-17A (IL-17A), and endothelial inflammation. Administration of anti-IL-17A antibodies to CD200R1-deficient mice normalized thrombin-antithrombin complexes in vivo, and a meta-analysis of human COVID-19 studies showed reduced pulmonary thromboembolism in those on anti-IL-17A antibodies. These findings highlight the utility of plasma proteomics to improve prediction of thrombosis in patients with cancer and to identify unanticipated mechanistic insights and therapeutic targets in thrombo-inflammatory disease. - Source: PubMed
Publication date: 2026/06/17
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