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Depletion of Specific Cell Populations by Complement Depletion
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Separation of self from non-self in the complement system.

J P Atkinson1, T Farries

  • 1Howard Hughes Medical Institute Laboratories and Department of Medicine, Division of Rheumatology, Washington University School of Medicine, St Louis, MO 63110, USA.

Immunology Today
|October 8, 2014
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Summary
This summary is machine-generated.

The alternative complement pathway distinguishes self from non-self using regulatory proteins. These inhibitors prevent excessive complement activation on host tissues while allowing defense against microbes.

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Area of Science:

  • Immunology
  • Molecular Biology

Background:

  • The alternative complement pathway is crucial for host defense against microbes.
  • This pathway must differentiate between self and non-self tissues.
  • Continuous low-grade activation (tickover) of C3 is a key feature.

Purpose of the Study:

  • To discuss the inhibitors of complement activation.
  • To explain how these regulators enable self-tolerance within the alternative complement pathway.

Main Methods:

  • Review and discussion of existing literature on complement regulation.
  • Analysis of the roles of plasma and membrane-bound glycoproteins.

Main Results:

  • Complement activation is initiated non-discriminately but amplified selectively.
  • Plasma and membrane-bound glycoproteins down-regulate complement activation on self-tissues.
  • These regulatory molecules are essential for preventing autologous tissue damage.

Conclusions:

  • The alternative complement pathway's ability to amplify on foreign tissue while being downregulated on autologous tissue is explained by these inhibitory molecules.
  • These regulators are critical for maintaining immune homeostasis and preventing autoimmune responses.