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Contribution of Adipose-Derived Factor D/Adipsin to Complement Alternative Pathway Activation: Lessons from

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Adipose tissue is the primary source of Factor D (FD), crucial for complement alternative pathway (AP) function. Even low levels of FD are sufficient for a functional AP, suggesting FD inhibition is a key therapeutic strategy.

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Area of Science:

  • Immunology
  • Metabolic Diseases

Background:

  • Factor D (FD) is a serine protease essential for the alternative pathway (AP) of the complement system.
  • Unlike most complement components, FD is predominantly produced by adipose tissue, making it a unique pharmaceutical target.

Purpose of the Study:

  • To determine the contribution of adipose tissue to circulating Factor D levels.
  • To ascertain the minimum quantity of FD required for a functional AP.

Main Methods:

  • Studied lipodystrophy mouse models (complete and partial), FD-deficient mice, and lipodystrophic patient samples.
  • Utilized serum mixing experiments, FD reconstitution, and adipose precursor transplantation.
  • Assessed AP function in various experimental conditions.

Main Results:

  • Complete lipodystrophy in mice led to undetectable FD and minimal AP activity.
  • Low serum FD levels were sufficient for normal AP activity in mice.
  • FD levels were reduced by approximately 50% in lipodystrophic patients.
  • Significant AP activity was observed even with small amounts of FD in humans and mice.

Conclusions:

  • Adipose tissue is the main source of serum FD in mice.
  • A low concentration of FD is sufficient for maintaining AP function.
  • Targeting FD for inhibition holds potential for treating autoimmune and inflammatory diseases driven by AP activation.