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Related Concept Videos

Complement System01:27

Complement System

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 membrane...
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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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Synergism is a useful mechanism where combining two or more drugs is more effective than each constituent used alone. Such combinations are also called supra-additive interactions. The drugs collectively enhance the final therapeutic effect by acting on different targets. Another advantage is that the low dose of each constituent drug is sufficient to achieve the desired effect. This helps reduce the duration of therapy and lower the adverse effects of these drugs.
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Aminoglycosides constitute a highly potent class of bactericidal antibiotics that exert their antimicrobial effects by targeting the bacterial ribosome, specifically disrupting protein synthesis. These polycationic molecules consist of amino-modified sugars linked via glycosidic bonds to an aminocyclitol core such as 2-deoxystreptamine or streptamine. Their strong positive charges facilitate tight binding to the negatively charged phosphate backbone of ribosomal RNA (rRNA), primarily at the 16S...
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Drugs target macromolecules to modify ongoing cellular processes. Primary drug targets include receptors, ion channels, transporters, and enzymes.
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Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...

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Depletion of Specific Cell Populations by Complement Depletion
06:17

Depletion of Specific Cell Populations by Complement Depletion

Published on: February 5, 2010

Drugs that inhibit complement.

Hubert Schrezenmeier1, Britta Höchsmann

  • 1German Red Cross Blood Transfusion Service Baden-Württemberg-Hessia, Institute of Clinical Transfusion Medicine and Immunogenetics Ulm, and University of Ulm, Helmholtzstraße 10, 89081 Ulm, Germany. h.schrezenmeier@blutspende.de

Transfusion and Apheresis Science : Official Journal of the World Apheresis Association : Official Journal of the European Society for Haemapheresis
|December 16, 2011
PubMed
Summary
This summary is machine-generated.

The complement system, vital for innate immunity, has a new targeted therapy, eculizumab, for paroxysmal nocturnal hemoglobinuria (PNH). This review updates its use and explores other complement-related disorders and novel inhibition strategies.

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Area of Science:

  • Immunology
  • Hematology
  • Pharmacology

Background:

  • The complement system is a critical component of innate immunity involved in numerous disease processes.
  • Targeted inhibition of complement factors has been limited until recently.
  • Eculizumab represents a significant advancement as a targeted therapy.

Purpose of the Study:

  • To review the clinical experience with eculizumab in paroxysmal nocturnal hemoglobinuria (PNH).
  • To discuss the potential applications of eculizumab in other complement-mediated disorders.
  • To explore emerging strategies for complement inhibition beyond eculizumab.

Main Methods:

  • Review of existing literature and clinical data on eculizumab.
  • Analysis of eculizumab's mechanism of action as a complement factor C5 inhibitor.
  • Exploration of therapeutic targets in other hematological and immunological conditions.

Main Results:

  • Eculizumab is an approved, disease-modifying treatment for PNH, inhibiting complement factor C5.
  • Significant clinical benefits of eculizumab in PNH patients have been documented since its 2007 approval.
  • Potential efficacy in conditions like cold agglutinin disease and atypical hemolytic uremic syndrome (aHUS) is under investigation.

Conclusions:

  • Eculizumab has transformed PNH treatment by targeting the complement system.
  • Further research is warranted to expand the therapeutic utility of eculizumab and other complement inhibitors.
  • Novel approaches to complement inhibition hold promise for various immune-related disorders.