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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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Hypersensitivity Reactions: Cytolytic Reactions01:01

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Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...
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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.
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Blood Typing01:10

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Understanding an individual's blood group is a critical component of transfusion medicine. It ensures compatibility in blood transfusions, organ transplants, and even during pregnancy. Determining these blood groups involves the ABO and Rh blood typing systems, utilizing specific antigens and corresponding anti-sera to identify an individual's blood type.
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Blood transfusion is a therapeutic measure to restore the blood volume after extensive blood loss due to an accident or a medical procedure. Blood transfusion involves drawing a certain amount of blood from a suitable donor and infusing it into the recipient.
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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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Complement in hemolytic anemia.

Robert A Brodsky1

  • 1Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.

Blood
|November 20, 2015
PubMed
Summary
This summary is machine-generated.

The complement system drives hemolytic anemias like paroxysmal nocturnal hemoglobinuria (PNH) and cold agglutinin disease (CAD), and thrombotic microangiopathy (TMA) in atypical hemolytic uremic syndrome (aHUS). Complement inhibitors are key treatments.

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Area of Science:

  • Immunology
  • Hematology
  • Pathophysiology

Background:

  • The complement system is increasingly implicated as a key driver in various human diseases.
  • Specific complement-mediated hemolytic anemias include paroxysmal nocturnal hemoglobinuria (PNH) and cold agglutinin disease (CAD).
  • Atypical hemolytic uremic syndrome (aHUS) involves complement-driven thrombotic microangiopathy (TMA).

Purpose of the Study:

  • To discuss the pathophysiology, diagnosis, and therapy of PNH, aHUS, and CAD.
  • To highlight the role of complement dysregulation in these hematologic disorders.
  • To review emerging diagnostic and therapeutic strategies, including complement inhibitors.

Main Methods:

  • Review of current literature on complement-mediated hemolytic anemias and TMA.
  • Discussion of the molecular mechanisms underlying PNH, aHUS, and CAD.
  • Analysis of diagnostic challenges and advancements, particularly for distinguishing aHUS from other TMAs.
  • Overview of therapeutic approaches, focusing on complement inhibition.

Main Results:

  • PNH pathophysiology involves loss of complement regulatory proteins CD59 and CD55, leading to red cell hemolysis.
  • aHUS is often caused by mutations activating the alternative complement pathway, resulting in TMA.
  • CAD involves IgM autoantibodies activating complement, causing extravascular hemolysis.
  • Distinguishing aHUS from other TMAs is crucial for effective therapy, with new bioassays under development.

Conclusions:

  • Complement system dysregulation is central to the pathogenesis of PNH, aHUS, and CAD.
  • Targeting complement activation with specific drugs is an effective therapeutic strategy for these conditions.
  • Continued research into diagnostics and therapeutics is vital for managing complement-mediated hematologic diseases.