Complement component C1q receptor (CD93) (C1qR)

Complement component C1q receptor (CD93) is a type I transmembrane glycoprotein primarily expressed on endothelial cells, myeloid cells, and platelets. Although originally identified as a receptor for the C1q subcomponent of the first complement component, its primary physiological role is now understood to be the regulation of angiogenesis and vascular integrity through interactions with extracellular matrix proteins such as multimerin-2 (MMRN2) and IGFBP7. CD93 is highly upregulated in the vasculature of various solid tumors, where it promotes the formation of dysfunctional, leaky blood vessels that contribute to tumor hypoxia and impaired immune cell infiltration. Therapeutic targeting of CD93 with monoclonal antibodies aims to normalize tumor vasculature, thereby improving drug delivery and enhancing the efficacy of immune checkpoint inhibitors. Additionally, CD93 plays a role in the clearance of apoptotic cells (efferocytosis) and is implicated in inflammatory and neurodegenerative conditions, including Alzheimer's disease, where it may influence synaptic pruning and neuroinflammation. While CD93 is the canonical C1qR, other proteins such as C1QBP (gC1qR) and calreticulin (cC1qR) also function as C1q-binding receptors in different cellular contexts.

Other names

CD93C1qRpC1QR1CDw93MXRA4AA4Complement component 1 q subcomponent receptor 1

Inhibition of CD93-MMRN2 interaction, vascular normalization, and enhancement of T-cell infiltration