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Immunology · Innate Immunity

Complement component receptors

Complement component receptors are specialized protein molecules on the surface of various cells in the body. They bind fragments of the complement system, mediating crucial immune responses such as opsonization, phagocytosis, clearance of immune complexes, and chemotaxis.

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Main roleProvide opsonization and engulfment of pathogens.
Major ligandsCleaved fragments of C3 and C4 components (C3b, iC3b, C4b).
AnaphylatoxinsC3aR and C5aR receptors mediate mediator release and chemotaxis.
Pathogen interactionCR2 serves as a receptor for Epstein–Barr virus binding.
2 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Main receptors and their ligands

Several types of receptors recognizing activated complement components are expressed on the membranes of human cells. Each of them has specific functions and distribution.

  • CR1 (CD35). Binds C3b, iC3b, C4b, C3d. Found on erythrocytes, monocytes, and macrophages. Participates in opsonization and clearance of immune complexes.
  • CR2 (CD21). Recognizes iC3b, C3dg, C3d. Present on B and T lymphocytes, as well as natural killer cells. Important for immunoregulation.
  • CR3 (CD11b/CD18) and CR4 (CD11c/CD18). Their main ligand is iC3b (along with C3b and C3dg for CR4). Located on phagocytes (monocytes/macrophages, neutrophils) and are responsible for opsonization.
  • Anaphylatoxin receptors (C3aR, C5aR, C5L2). Bind small fragments C3a and C5a. Found on granulocytes and monocytes, providing chemotaxis and degranulation.

Molecular mechanisms of phagocytosis

The process of particle engulfment by a phagocyte begins with the binding of the target to membrane receptors. Although signal transduction pathways may vary (e.g., for complement or antibody receptors), the end result is always the internalization and destruction of the foreign agent.

  1. A temporary structure forms on the phagocyte surface—the phagocytic cup (phagocytic cup).
  2. Receptors cluster together, causing a change in their conformation.
  3. An intracellular cascade is triggered involving Src and Syk family kinases, which phosphorylate tyrosine residues in the receptors.
  4. Further signal transduction requires key enzymes: phosphoinositide 3-kinase (PI3K) and phospholipase C (PLC). Without them, the progression of phagocytosis is impossible.
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Role of the cytoskeleton and GTPases

For a phagocyte to change shape and engulf a target, rearrangement of its actin cytoskeleton is necessary. This process is tightly regulated by specialized proteins—GTPases.

  • In complement-dependent phagocytosis (via C3R receptors), the activity of the Rho GTPase predominates.
  • Polymerization of actin filaments requires guanine nucleotide exchange factors (GEFs), such as the Vav protein.
  • Activation of the Arp complex, which ensures actin assembly, occurs with the mandatory participation of the WASP protein.

Failures at this stage lead to severe consequences. For example, a genetic defect in the WASP protein disrupts normal actin polymerization, which clinically manifests as a primary immunodeficiency—Wiskott–Aldrich syndrome.

Briefly: answers to topical questions

What non-complement ligands can the CR3 (CD11b/CD18) receptor bind?

The CR3 receptor (CD11b/CD18), also known as Mac-1 or integrin αMβ2, is capable of binding fibrinogen and heparin among non-complement ligands.

According to the cited sources, ligands for CR3 include:

  • iC3b—a complement fragment;
  • fibrinogen;
  • heparin, etc.

Class and exam questions

Which cells predominantly express the CR1 receptor?

CR1 (CD35) is expressed predominantly on erythrocytes, monocytes, and macrophages.

For which virus is the CR2 receptor the entry portal?

The CR2 receptor (CD21) mediates the binding of the Epstein–Barr virus.

What disease does a WASP protein defect lead to?

WASP protein dysfunction causes Wiskott–Aldrich syndrome, a severe primary immunodeficiency.

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What else to study on this topic

  • Detailed mechanism of Src and Syk kinase activation
  • The role of phosphoinositide 3-kinase (PI3K) in phagocytosis
  • DAG formation and protein kinase C (PKC) activation
  • Signaling pathways from FcR receptors (RAC1, Cdc42)
  • Functions of WAVE, PAK1, and ROCK proteins in cytoskeletal rearrangement

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