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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 and Agglutination

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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.

Hematology. American Society of Hematology. Education Program
|December 6, 2015
PubMed
Summary
This summary is machine-generated.

Complement activation drives diseases like paroxysmal nocturnal hemoglobinuria (PNH), atypical hemolytic uremic syndrome (aHUS), and cold agglutinin disease (CAD). Complement inhibitors are emerging as key therapies for these conditions.

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Area of Science:

  • Immunology
  • Hematology
  • Pathophysiology

Background:

  • Complement system activation is implicated in various human diseases.
  • Deficiencies in complement regulatory proteins (CD59, CD55) cause susceptibility to hemolysis in paroxysmal nocturnal hemoglobinuria (PNH).
  • Mutations leading to alternative complement pathway activation cause thrombotic microangiopathy (TMA) in atypical hemolytic uremic syndrome (aHUS).

Purpose of the Study:

  • To discuss the pathophysiology, diagnosis, and therapy of PNH, aHUS, and CAD.
  • To highlight the role of complement in hemolytic anemias and TMA.
  • To review the development of novel bioassays for distinguishing aHUS from other TMAs.

Main Methods:

  • Review of current literature on complement-mediated diseases.
  • Discussion of diagnostic criteria for PNH, aHUS, and CAD.
  • Overview of therapeutic strategies, including complement inhibitors.

Main Results:

  • Paroxysmal nocturnal hemoglobinuria (PNH) involves complement-mediated red blood cell destruction due to loss of regulatory proteins.
  • Atypical hemolytic uremic syndrome (aHUS) is characterized by TMA driven by complement pathway activation.
  • Cold agglutinin disease (CAD) involves IgM autoantibodies activating complement, leading to hemolysis.

Conclusions:

  • Complement plays a critical role in the pathogenesis of PNH, aHUS, and CAD.
  • Distinguishing aHUS from other TMAs is crucial for effective treatment.
  • Therapeutic strategies targeting complement activation are increasingly important for managing these hematologic disorders.