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The pathobiology of the terminal complement complexes.

A P Dalmasso1, R J Falk, L Raij

  • 1Department of Laboratory Medicine and Pathology, Veterans Administration Medical Center, Minneapolis, Minn.

Complement and Inflammation
|January 1, 1989
PubMed
Summary
This summary is machine-generated.

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The terminal complement pathway forms C5b-9 complexes, which, beyond cell lysis, trigger cellular activities. Detecting these complexes in tissues and fluids aids in understanding and potentially diagnosing diseases like SLE nephritis and rheumatoid arthritis.

Area of Science:

  • Immunology
  • Molecular Biology
  • Pathology

Background:

  • The terminal complement pathway generates C5b-9 and SC5b-9 complexes.
  • Sublytic C5b-9 activates cellular functions beyond direct cell lysis.
  • These complexes are implicated in various pathological conditions.

Purpose of the Study:

  • To investigate the role and detection of terminal complement complexes (TCC) in disease.
  • To explore the diagnostic potential of TCC and related autoantibodies.

Main Methods:

  • Utilized antibodies recognizing C9 neoantigens to detect TCC deposits in human tissues.
  • Developed methods for measuring soluble SC5b-9 in biological fluids.
  • Assessed autoantibodies against C9 neoantigens in patient plasma.

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Main Results:

  • TCC deposits found in both immunological and non-immunological diseases, sometimes without immunoglobulin or C3 co-deposition.
  • Elevated SC5b-9 levels observed in SLE nephritis, infections, cardiopulmonary bypass, CNS inflammatory diseases, and rheumatoid arthritis.
  • Autoantibodies to C9 neoantigens identified in patients with autoimmune, infectious, and neoplastic diseases.

Conclusions:

  • TCC play a role in various pathological conditions, with potential diagnostic implications.
  • SC5b-9 levels and C9 neoantigen autoantibodies may serve as biomarkers for disease activity and diagnosis.
  • Further research is needed to fully establish the clinical utility of these findings.