The gene C5AR1 encodes the complement component 5a receptor 1 (C5aR1, CD88), a principal member of the G protein-coupled receptor (GPCR) family. C5aR1 functions as the high-affinity receptor for the potent complement anaphylatoxin C5a, transducing its inflammatory and chemotactic signals ^[1]. The receptor exhibits broad expression, particularly enriched on cells of the innate immune system, including neutrophils, monocytes, macrophages, and dendritic cells, with detectable expression also noted on endothelial, epithelial, and smooth muscle cells ^[2]. Upon engagement with C5a, C5aR1 couples to G proteins and recruits β-arrestin, activating intracellular signaling cascades that orchestrate diverse cellular responses such as directed migration, degranulation, oxidative burst, and the synthesis of pro-inflammatory mediators ^[2-3]. Dysregulated C5aR1 signaling is a critical factor in the pathogenesis of numerous inflammatory and autoimmune disorders, including sepsis, rheumatoid arthritis, inflammatory bowel disease, and psoriasis, and is implicated in neuroinflammatory conditions such as Alzheimer's disease, as well as contributing to the tumor microenvironment ^[3-4]. Given its pivotal role in mediating C5a-driven inflammation, C5aR1 has emerged as a compelling therapeutic target, with pharmacological modulators currently undergoing investigation for various clinical applications.

The B6-hC5AR1 mouse is a humanized model constructed by replacing the partial intron 1 to TAG stop codon of the mouse C5ar1 gene in situ with the corresponding sequence from the human C5AR1 gene. B6-hC5AR1 mice can be used for the research on the pathogenesis of various inflammatory diseases such as psoriasis, rheumatoid arthritis, and inflammatory bowel disease, neuroinflammation related to Alzheimer's disease, and some tumors, as well as for C5AR1-targeted drug development.