Membrane immune adherence receptor that plays a critical role in the capture and clearance of complement-opsonized pathogens by erythrocytes and monocytes/macrophages (PubMed:2963069). Mediates the binding by these cells of particles and immune complexes that have activated complement to eliminate them from the circulation (PubMed:2963069). Acts also in the inhibition of spontaneous complement activation by impairing the formation and function of the alternative and classical pathway C3/C5 convertases, and by serving as a cofactor for the cleavage by factor I of C3b to iC3b, C3c and C3d,g, and of C4b to C4c and C4d (PubMed:2972794, PubMed:8175757). Also plays a role in immune regulation by contributing, upon ligand binding, to the generation of regulatory T cells from activated helper T cells (PubMed:25742728). (Microbial infection) Acts as a receptor for Epstein-Barr virus. Interacts (via Sushi 1 and Sushi 2 domains) with complement factor C4b (PubMed:2972794, PubMed:8175757). Interacts (via Sushi 8 and Sushi 9 domains) with complement factor C3b (PubMed:2972794, PubMed:8175757). Interacts (via Sushi 24 and Sushi 25 domains) with MBL2 (PubMed:23460739, PubMed:29563915). Interacts with FCN2 (PubMed:2972794). Interacts (via Sushi 24 and Sushi 25 domains) with C1QA (PubMed:9324355, PubMed:29563915). (Microbial infection) Interacts with Epstein-Barr virus gp350. Present on erythrocytes, a subset of T cells, mature B cells, follicular dendritic cells, monocytes and granulocytes. CR1 contains a system of antigens called the Knops blood group system. Polymorphisms within this system are involved in malarial rosetting, a process associated with cerebral malaria, the major cause of mortality in Plasmodium falciparum malaria. Common Knops system antigens include McCoy (McC) and Sl(a)/Vil (Kn4, or Swain-Langley; Vil or Villien). Sl(a-) phenotype is more common in persons of African descent and may protect against fatal malaria. Other polymorphic forms of CR1 contain 23, 37 or 44 Sushi (CCP/SCR) domains instead of the 30 Sushi (CCP/SCR) domains. The most frequent alleles are the F allotype (shown here) and the S allotype (37 repeat Sushi domains). The gene frequencies of the F allotype and S allotype are 0.87 and 0.11 in Caucasians, 0.82 and 0.11 in African Americans, 0.89 and 0.11 in Mexicans. Genetic variations in CR1 resulting in CR1 deficiency are involved in protection against severe malaria [MIM:611162]. Parasitized red blood cells (RBCs) from children suffering from severe malaria often adhere to complement receptor 1 (CR1) on uninfected RBCs to form clumps of cells known as rosettes. CR1-deficient red blood cells show greatly reduced rosetting and CR1 deficiency occurs in healthy individuals from malaria-endemic regions. Belongs to the receptors of complement activation (RCA) family. Blood group antigen gene mutation database