Ask about this productRelated genes to: C5AR1 antibody
- Gene:
- C5AR1 NIH gene
- Name:
- complement C5a receptor 1
- Previous symbol:
- C5R1
- Synonyms:
- C5A, C5AR, CD88
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-04
- Date modifiied:
- 2016-08-10
Related products to: C5AR1 antibody
Related articles to: C5AR1 antibody
- Kawasaki disease (KD) is an acute febrile systemic vasculitis of unknown etiology and the leading cause of acquired heart disease among children. Complement activation has long been observed in patients with acute KD, however, its contribution to disease development remains unknown. Here, using publicly available datasets, we showed that patients with acute KD exhibited higher expression of complement products in whole blood, consistent with the activation of the complement pathway. Similarly, in the Lactobacillus casei cell wall extract (LCWE) murine model of KD, LCWE injection induced increased expression of complement products in cardiovascular tissues, suggestive of activation of the complement pathways. C3-deficient mice or WT mice treated with the complement C5a Receptor 1 (C5ar1) antagonist developed significantly more severe LCWE-induced cardiovascular lesions and vasculitis. Furthermore, we observed that LCWE binds to serum C3, an opsonizing factor that labels microbial targets for clearance, and LCWE deposition in the liver was significantly higher in C3-deficient mice compared to WT mice. Overall, our data indicate that blocking the complement system significantly exacerbates LCWE-induced KD vasculitis, likely by impairing C3-mediated clearance of LCWE. These data suggest that the complement pathway may play a protective role in KD pathogenesis by promoting clearance of potential bacterial or viral trigger of KD. - Source: PubMed
Publication date: 2026/05/12
Atici Asli EKocatürk BegümRoss Benjamin LAubuchon Emily APorritt Rebecca ACarvalho Thacyana TNamba TakahiroLee YounghoNoval Rivas MagaliArditi Moshe - The lymphatic system is a highly branched endothelial tubular network that facilitates the migration of immune cells from the peripheral tissues to lymph nodes (LNs) and other lymphoid organs. Complement factors are essential for innate and adaptive immune functions. Complement anaphylatoxin C5a is crucial in vascular endothelial cell activation and lymphocyte polarization. Understanding the impact of C5a and its cognate receptor C5ar1 signaling on lymphatic function could provide new insights into the mechanisms of immune dysregulation observed in chronic inflammatory diseases. We demonstrate that acute C5a challenge in wildtype C57B6/J mice significantly reduced lymph propulsion compared to their C5ar1-deficient counterparts. C5ar1-dependent attenuation of lymph propulsion with LPS challenge corroborated with significantly increased endothelial-derived inducible nitric oxide synthase (iNOS) expression. C5ar1-iNOS axis modulated T helper cell polarization towards Cd4/Ccr5 Th1 subtypes, indicating that C5a-activated endothelial-iNOS may contribute to Th1 polarization in the peripheral LNs during homing. Finally, we observed C5a-mediated endothelial surface glycoprotein CD146 interaction with Th1 cell intermediate filament protein vimentin that may facilitate transmigration of activated Th1 cells into systemic circulation and tissue interstitium. Given the critical role of the C5a/C5ar1 axis in promoting lymphatic dysfunction, our study highlights the therapeutic potential of targeting C5ar1 in chronic inflammatory conditions. - Source: PubMed
Publication date: 2026/02/10
Rich Haydn ELi Yi-DongHok Kathryn DMueller-Ortiz Stacey LDomozhirov Aleksey YShadid AnthonyThandavarayan Rajarajan AYalamanchili Hari KrishnaDoursout Marie-FrancoiseWeng-Mills TingtingBishehsari FarazBanda Nirmal KEckel-Mahan Kristin LRestrepo Marcos IShivshankar Pooja - Hepatic ischemia-reperfusion injury (HIRI) is an unavoidable complication of liver transplantation (LT) that drives allograft dysfunction and mortality. Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) show therapeutic promise, yet their actions within the hepatic network remain incompletely defined. We investigated how MSC-EVs protect against LT-induced HIRI, focusing on intercellular communication and complement-mediated inflammation. - Source: PubMed
Publication date: 2026/05/05
Liu YasongXiao JiaqiWu ZhengqiZhang FengYou QiangChen HaitianZhang JiebinYang YangWang TingtingYi ShuhongLi RongZheng Jun - Neutrophil extracellular traps are implicated in immunothrombosis and neuroinflammation in ischemic stroke, but blood-based markers that distinguish subtype-specific thromboinflammatory patterns remain limited. We applied an integrated multi-omics strategy combining multi-cohort peripheral-blood transcriptomics, machine-learning feature selection, Mendelian randomization, and single-cell RNA sequencing, followed by in silico perturbation analyses and compound prioritization with molecular docking, molecular dynamics simulation, and cellular thermal shift assays. Plasma citrullinated histone H3 levels were elevated across ischemic stroke subtypes and were highest in cardioembolic stroke. Integrative transcriptomic analysis identified a 7-gene neutrophil extracellular trap-related diagnostic signature comprising PADI4, C5AR1, MMP9, LRG1, NFIL3, TREM1, and PGLYRP1, with good cross-cohort diagnostic performance (area under the curve 0.789-0.834). Among these genes, MMP9 showed a broad association across ischemic stroke cohorts, whereas PGLYRP1 showed a cardioembolic stroke-enriched signal and a putative causal association with cardioembolic stroke in Mendelian randomization analyses. Two-step mediation analyses did not support a significant mediating role for the tested systemic cytokines, consistent with a more localized thromboinflammatory context. Single-cell computational perturbation suggested that Pglyrp1 may influence neutrophil-associated programs and intercellular communication. Molecular dynamics simulations prioritized Naringin as a candidate MMP9-binding compound, and cellular thermal shift assays supported cellular target engagement for the MMP9-Naringin pair. These findings provide a neutrophil extracellular trap-centered framework for biologically informed stratification of ischemic stroke and nominate MMP9 and PGLYRP1 as candidate biomarkers and therapeutic hypotheses for further validation. - Source: PubMed
Publication date: 2026/04/30
Tan HaozhouGong HaoyuLi HuiHuang MengyaoZhang JingyuanLiu YanLi YingSong YuanjianFeng Qian - Allogeneic hematopoietic stem cell microtransplantation (MST) has been shown in prior studies to improve outcomes compared to chemotherapy alone in acute myeloid leukemia, but its mechanism requires further investigation. In MST, donor peripheral blood mononuclear cells (GPBMCs) mobilized by granulocyte colony-stimulating factor (G-CSF), which contain a large number of NK cells, are infused after each chemotherapy cycle (typically 3-5 infusions total). - Source: PubMed
Publication date: 2026/04/24
Zhang Tian-YaoLiu Ru-YuLei Yang-YangCai BoYu Chang-LinGuo MeiAi Hui-ShengWang YiHu Kai-Xun