Complement Component C3a Receptor (C3AR1) Antibody

Background

C3AR1 is a G protein-coupled receptor that binds C3a, a complement system-derived anaphylatoxin, playing a pivotal role in inflammation and immune responses. C3AR1 is widely expressed on immune cells, including neutrophils, macrophages, eosinophils, and mast cells, where it mediates chemotaxis, degranulation, and cytokine production in response to C3a binding. It is a key regulator of the complement system, promoting immune cell recruitment and activation during infections, injury, and inflammatory responses. C3AR1 signaling activates pathways such as PI3K/Akt and ERK, driving cellular responses that contribute to host defense. Dysregulated C3AR1 activity is implicated in inflammatory and autoimmune diseases, including rheumatoid arthritis, asthma, and sepsis, where excessive complement activation exacerbates tissue damage and inflammation. In cancer, C3AR1 expression on tumor-associated macrophages and other immune cells modulates the tumor microenvironment, promoting immunosuppression and angiogenesis. C3AR1 is also involved in neuroinflammation, contributing to neurodegenerative diseases like Alzheimer’s and multiple sclerosis by mediating microglial activation and cytokine release. Therapeutically, targeting C3AR1 with inhibitors or antagonists is being explored to modulate complement-driven inflammation and reduce tissue damage in autoimmune diseases and cancer.