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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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Defense Against Bacterial Pathogens01:31

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The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
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Antimicrobial proteins are important components of the immune system. They aid the body in combating pathogens by either killing them directly or hindering their replication processes. Four main types of antimicrobial substances are interferons, the complement system, iron-binding proteins, and antimicrobial proteins.
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What is the Immune System?01:38

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Antibody Actions01:26

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Antibodies, or immunoglobulins, are critical players in the immune system's arsenal against invading pathogens. Produced by B cells and plasma cells, their primary role is to detect and bind to specific antigens, molecules found on the surface of pathogens like bacteria or viruses. Beyond antigen recognition, antibodies perform several vital functions that contribute to immune defense.
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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.
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Updated: Apr 18, 2026

Depletion of Specific Cell Populations by Complement Depletion
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Depletion of Specific Cell Populations by Complement Depletion

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Molecules Great and Small: The Complement System.

Douglas R Mathern1, Peter S Heeger2

  • 1Translational Transplant Research Center, Department of Medicine, Recanati Miller Transplant Institute, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, New York.

Clinical Journal of the American Society of Nephrology : CJASN
|January 9, 2015
PubMed
Summary
This summary is machine-generated.

The complement system, once seen as solely for immunity, is now a key player in kidney disease. Targeting complement offers a promising new approach to treat various kidney conditions and improve patient outcomes.

Keywords:
GNcomplementimmunologytransplantation

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Area of Science:

  • Immunology
  • Nephrology
  • Complement System Biology

Background:

  • The complement cascade is increasingly recognized for its pathogenic role in kidney diseases, moving beyond its traditional function in innate immunity.
  • Complement activation is implicated in antibody-mediated kidney transplant rejection, glomerulonephritis (GN), C3 nephropathies, and atypical hemolytic uremic syndrome.
  • Local complement production by kidney cells and immune cells contributes to ischemia-reperfusion injury, fibrosis, and T cell-mediated kidney diseases.

Purpose of the Study:

  • To review the multifaceted roles of the complement system in the pathogenesis of diverse kidney diseases.
  • To highlight the emerging understanding of complement's contribution to T cell-mediated immunity and kidney inflammation.
  • To discuss the therapeutic potential of targeting complement pathways for kidney disease treatment.

Main Methods:

  • Review of current literature and emerging data on complement's role in kidney disease.
  • Analysis of complement activation pathways (classical, mannose-binding lectin, alternative) and their mediators (C3a, C5a).
  • Examination of complement production by various cells, including liver, endothelial, tubular, and immune cells.

Main Results:

  • Complement activation is central to kidney transplant rejection and various forms of GN (membranous GN, anti-GBM disease, lupus nephritis).
  • Dysregulation of complement regulators contributes to C3 nephropathies and atypical hemolytic uremic syndrome.
  • Immune cell-derived complement enhances pathogenic T cell responses, promoting transplant rejection and potentially other T cell-mediated kidney diseases.
  • Complement activation, particularly C5a/C5aR signaling, drives vascular inflammation in ANCA-associated renal vasculitis.

Conclusions:

  • The complement system is a critical mediator in a wide spectrum of kidney diseases.
  • Targeting complement components and receptors presents a promising therapeutic strategy to halt kidney disease progression.
  • Translational research and pharmacologic development are paving the way for novel complement-targeted therapies in nephrology.