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Related Concept Videos

Complement System01:27

Complement System

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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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Complementation Tests00:49

Complementation Tests

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A complementation test is a simple cross to identify whether the two mutations are located on the same gene or different genes. It was first performed by Edward Lewis in the 1940s while working on fruit flies. He developed the test to identify the location and arrangement of different mutations on chromosomes.
Organisms heterozygous for different mutations are crossed pairwise in all combinations. If present on different genes, the mutations can complement each other by providing the missing...
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Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation01:21

Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation

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Clinical manifestationsPeripheral Arterial Disease (PAD) manifests through a range of symptoms, from the characteristic intermittent claudication to atypical presentations and severe complications in advanced stages. Intermittent claudication, a hallmark symptom of PAD, presents as exercise-induced muscle pain that typically resolves within minutes of rest. This pain is reproducible and stems from inadequate blood flow, leading to the accumulation of lactic acid produced during anaerobic...
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Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

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Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum...
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Humoral Immune Responses01:36

Humoral Immune Responses

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Overview
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Related Experiment Video

Updated: Mar 26, 2026

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
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Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

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Diagnosis of complement alternative pathway disorders.

Andrea Angioi1, Fernando C Fervenza1, Sanjeev Sethi2

  • 1Division of Nephrology and Hypertension, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.

Kidney International
|January 26, 2016
PubMed
Summary
This summary is machine-generated.

Abnormal complement alternative pathway control causes kidney diseases like atypical hemolytic uremic syndrome. Comprehensive biochemical, genetic, and pathologic analysis aids diagnosis and targeted treatment for these complement alternative pathway disorders.

Keywords:
C3 glomerulopathyC3 glomerulonephritisalternative pathwayatypical hemolytic uremic syndromeclassical pathwaycomplementdense-deposit diseaseglomerulonephritis

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Measuring Erythrocyte Complement Receptor 1 Using Flow Cytometry
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Area of Science:

  • Nephrology
  • Immunology
  • Genetics

Background:

  • Kidney diseases such as atypical hemolytic uremic syndrome, C3 glomerulonephritis, dense-deposit disease, and atypical postinfectious glomerulonephritis stem from aberrant complement alternative pathway regulation.
  • These diverse conditions share a common etiology: impaired complement control due to genetic or acquired defects in the alternative pathway.

Purpose of the Study:

  • To outline a unified diagnostic strategy for kidney diseases linked to complement alternative pathway dysregulation.
  • To emphasize the importance of comprehensive analysis for identifying specific defects and guiding treatment.

Main Methods:

  • Biochemical assessment including functional complement pathway activity, component/regulator analysis, and activation product quantification.
  • Genetic analysis to identify causative mutations in complement alternative pathway genes.
  • Pathologic examination of kidney biopsies using immunofluorescence and laser microdissection with mass spectrometry.
  • ADAMTS-13 activity testing to differentiate from thrombotic thrombocytopenic purpura in thrombotic microangiopathy cases.

Main Results:

  • The diagnostic approach involves a multi-faceted analysis of the complement alternative pathway.
  • The genetic landscape of these disorders is continually expanding.
  • Advanced techniques like laser microdissection with mass spectrometry enhance pathologic analysis.

Conclusions:

  • A comprehensive diagnostic workup is essential for identifying the specific defect in the complement alternative pathway.
  • Pinpointing the underlying cause enables precise, targeted therapeutic interventions for improved patient outcomes.