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Related Experiment Videos

Detection of complement in relation to disease.

M M Frank1

  • 1Department of Pediatrics, Duke University Medical Center, Durham, N.C. 27710.

The Journal of Allergy and Clinical Immunology
|March 1, 1992
PubMed
Summary
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Complement activation.

Immunology today·2014
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Wild-type adenoviruses from groups A-F evoke unique innate immune responses, of which HAd3 and SAd23 are partially complement dependent.

Gene therapy·2008
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Recombinant adenovirus vectors activate the alternative complement pathway, leading to the binding of human complement protein C3 independent of anti-ad antibodies.

Molecular therapy : the journal of the American Society of Gene Therapy·2004
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Complement activation influences Staphylococcus aureus adherence to endothelial cells.

Infection and immunity·2003
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Availability of complement bound to Staphylococcus aureus to interact with membrane complement receptors influences efficiency of phagocytosis.

Infection and immunity·2003
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Complement 1 inhibitor is a regulator of the alternative complement pathway.

The Journal of experimental medicine·2001

Investigating low complement levels can reveal genetic defects or ongoing complement activation. Analyzing complement pathways and split products aids in diagnosing clinical conditions and understanding complement-mediated damage.

Area of Science:

  • Immunology
  • Clinical Medicine
  • Biochemistry

Background:

  • The complement system is a crucial part of innate immunity.
  • Dysregulation of the complement system can lead to various diseases.
  • Understanding complement activation pathways is essential for clinical diagnostics.

Purpose of the Study:

  • To explore the diagnostic implications of reduced complement component levels.
  • To investigate the role of complement activation in clinical settings.
  • To correlate complement pathway activation with specific diagnoses.

Main Methods:

  • Analysis of individual complement component titers.
  • Detection of complement split products and immune complexes.
  • Evaluation of complement pathway activation (classical vs. alternative).

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  • Family studies to assess genetic complement deficiencies.
  • Main Results:

    • Low levels of a single complement component may indicate a genetic defect.
    • Presence of split products or complexes suggests active complement consumption.
    • Reduced levels of multiple components often point to complement activation.
    • Identifying the activated pathway (classical or alternative) aids in differential diagnosis.

    Conclusions:

    • Hypocomplementemia can be indicative of genetic disorders or active complement pathways.
    • Analysis of complement system components and activation patterns is valuable for diagnosing complement-related diseases.
    • Understanding complement pathophysiology aids in assessing its role in clinical damage.