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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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Related Experiment Video

Updated: Nov 10, 2025

A Precision Medicine Tool for Measurement and Monitoring of Hemoglobin S in Sickle Cell Disease Patients Receiving Transfusion Therapy
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Complement in Sickle Cell Disease: Are We Ready for Prime Time?

Christos Varelas1, Athina Tampaki2, Ioanna Sakellari1

  • 1Hematology Department - BMT Unit, G. Papanicolaou Hospital, Thessaloniki, Greece.

Journal of Blood Medicine
|April 1, 2021
PubMed
Summary

Sickle cell disease (SCD) involves complement activation, a key factor in its pathology. Understanding these mechanisms may lead to new treatments targeting complement inhibition for better patient outcomes.

Keywords:
complement inhibitioncomplement systemeculizumabsickle cell disease

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Area of Science:

  • Hematology
  • Immunology
  • Genetics

Background:

  • Sickle cell disease (SCD) is an inherited blood disorder characterized by sickle hemoglobin (HbS).
  • SCD leads to anemia, infections, and severe complications like vaso-occlusive crisis (VOC) and delayed hemolytic transfusion reaction (DHTR).
  • Current treatments, including hydroxyurea, improve outcomes but do not fully address disease pathology.

Purpose of the Study:

  • To review current data on complement activation in SCD patients.
  • To elucidate the mechanisms of complement over-activation in SCD.
  • To discuss therapeutic strategies, including complement inhibition, for SCD management.

Main Methods:

  • Literature review of studies on complement activation in sickle cell disease.
  • Analysis of pathophysiological mechanisms involving sickle cells, neutrophils, platelets, and endothelial cells.
  • Evaluation of existing and emerging therapeutic agents, including complement inhibitors.

Main Results:

  • Complement activation is implicated in SCD pathophysiology during both steady state and crisis.
  • The precise mechanisms governing complement over-activation in SCD require further elucidation.
  • Eculizumab has shown benefits in DHTR, with limited data for VOC; novel agents are in development.

Conclusions:

  • Complement activation plays a significant role in SCD pathogenesis.
  • Identifying patients who would benefit from complement inhibition is crucial for targeted therapy.
  • Novel therapeutic approaches, including complement inhibition, hold promise for improved SCD management.