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IgM-Dependent Phagocytosis in Microglia Is Mediated by Complement Receptor 3, Not Fcα/μ Receptor

Jonathan R Weinstein1, Yi Quan2, Josiah F Hanson2

  • 1Department of Neurology, School of Medicine, University of Washington, Seattle, WA 98195; jweinste@u.washington.edu.

Journal of Immunology (Baltimore, Md. : 1950)
|October 27, 2015
PubMed

Insights

Microglia use complement receptor 3 and C3 for Staphylococcus aureus phagocytosis, not Fcα/μR. This finding is crucial for understanding immune responses in central nervous system infections.

Area of Science:

  • Neuroimmunology
  • Infectious Diseases
  • Cell Biology

Background:

  • Microglia are key phagocytes in the central nervous system (CNS).
  • Bacterial opsonization with immunoglobulins (Igs) or complement facilitates microglial pathogen recognition and phagocytosis via Fc or complement receptors.
  • Fcα/μR, a receptor for IgM and IgA, is less understood in microglial function.

Purpose of the Study:

  • To investigate the role of Fcα/μR in microglial phagocytosis of opsonized bacteria.
  • To determine if Fcα/μR mediates IgM-enhanced phagocytosis of Staphylococcus aureus by microglia.

Main Methods:

  • Primary microglia and N9 microglial cells were used to assess Fcα/μR expression.
  • Phagocytosis assays were performed using Staphylococcus aureus and anti-Staphylococcus aureus IgM.
  • Experiments utilized Fcα/μR knockout (Fcα/μR(-/-)) mice microglia.
  • Complement receptor 3 (CR3) components (CD11b, CD18) and C3 were genetically or immunologically inactivated.

Main Results:

  • Microglia express Fcα/μR, and anti-Staphylococcus aureus IgM increased phagocytosis rates.
  • IgM-dependent phagocytosis of Staphylococcus aureus was not impaired in Fcα/μR(-/-) microglia.
  • Blocking CR3 (CD11b) reduced IgM-mediated phagocytosis of Staphylococcus aureus.
  • Phagocytosis was significantly reduced in microglia deficient in CD18 or C3.

Conclusions:

  • Complement receptor 3 and C3, not Fcα/μR, are implicated in IgM-mediated phagocytosis of Staphylococcus aureus by microglia.
  • These findings highlight the critical role of the complement system in microglial defense against bacterial infections in the CNS.

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