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Updated: Jan 10, 2026

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C1q-CD44 interactions regulate microglial phagocytosis, proliferation, and migration.

Pooja S Sakthivel1, Alyssa J Villegas1, Anita Lakatos1

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Complement protein C1q interacts with CD44 receptor on microglia to regulate phagocytosis, proliferation, and migration, impacting neurodegeneration. This C1q-CD44 interaction is key for microglial function in CNS health and disease.

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Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Microglia are central nervous system immune cells responding to neurodegeneration.
  • Complement protein C1q is implicated in aging and neurodegeneration.
  • Previous studies showed exogenous C1q affects human induced pluripotent stem cell-derived microglia (iMG) function.

Purpose of the Study:

  • To investigate the role of CD44 as a C1q receptor on iMG.
  • To determine if C1q-induced microglial changes are CD44-dependent.
  • To elucidate the functional consequences of C1q-CD44 interactions.

Main Methods:

  • Validated expression of C1q receptors (RNA and protein) on iMG.
  • Proximity ligation assay to confirm C1q-receptor binding.
  • Generated CD44 knockout iMG to assess C1q response dependency.

Main Results:

  • C1q-induced inflammatory response in iMG was not CD44-dependent.
  • C1q-CD44 interactions were shown to modulate microglial phagocytosis.
  • C1q-CD44 interactions regulate microglial proliferation and migration.

Conclusions:

  • C1q interacts with CD44 on iMG to modulate critical microglial functions.
  • These findings highlight C1q-CD44 interactions as important in CNS health and disease.
  • Further research will explore therapeutic potential of modulating C1q-CD44 interactions in neurodegeneration.