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Deficiencies of human C3 complement receptors type 1 (CR1, CD35) and type 2 (CR2, CD21)

M D Kazatchkine1, D T Fearon

  • 1Unité d'Immunopathologie and INSERM U28, Hôpital Broussais, Paris, France.

Immunodeficiency Reviews
|January 1, 1990
PubMed

Insights

Complement receptors 1 (CR1) and 2 (CR2) are key proteins involved in immune responses. This review details their molecular biology, functions, and altered expression in diseases like systemic lupus erythematosus.

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Complement receptors 1 (CR1/CD35) and 2 (CR2/CD21) are transmembrane glycoproteins crucial for the complement system.
  • CR1 binds C3b, while CR2 binds C3dg, playing roles in immune complex clearance and B-cell function.
  • These receptors are encoded by genes located in the RCA locus on chromosome 1.

Purpose of the Study:

  • To review the molecular biology and functional characteristics of CR1 and CR2.
  • To focus on the alterations in CR1 and CR2 expression in various diseases.
  • To emphasize genetic and acquired factors causing defective CR1 expression in systemic lupus erythematosus.

Main Methods:

  • Literature review of existing studies on CR1 and CR2.
  • Analysis of molecular structures and ligand-binding properties.
  • Examination of gene localization and expression patterns.

Main Results:

  • CR1 has broad cellular distribution, mediating immune complex transport, phagocytosis, IL-1 secretion, and B-cell differentiation.
  • CR2 is restricted to B lymphocytes and follicular dendritic cells, modulating B-cell growth and serving as the Epstein-Barr virus (EBV) receptor.
  • Defective CR1 expression in systemic lupus erythematosus is linked to genetic and acquired factors.

Conclusions:

  • CR1 and CR2 are vital for distinct immunological functions.
  • Altered expression of these receptors is implicated in disease pathogenesis.
  • Understanding these alterations, particularly for CR1 in SLE, is crucial for therapeutic strategies.

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