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Updated: Apr 11, 2026

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

Published on: January 29, 2014

Paroxysmal nocturnal hemoglobinuria: a complement-mediated hemolytic anemia.

Amy E DeZern¹, Robert A Brodsky²

¹Division of Hematologic Malignancies, Department of Oncology, The Bunting and Blaustein Cancer Research Building, 1650 Orleans Street, Room 3M87, Baltimore, MD 21287-0013, USA.

Hematology/Oncology Clinics of North America

|June 5, 2015

Summary

Paroxysmal nocturnal hemoglobinuria (PNH) involves complement-driven hemolysis, thrombosis, and marrow failure. Complement inhibition therapy improves outcomes but residual activity necessitates ongoing research into advanced strategies.

Keywords:

Alternative pathway of complement Bone marrow failure C1 inhibition C3 blockade Eculizumab Hemolytic anemia Humanized anti-C5 monoclonal antibody Paroxysmal nocturnal hemoglobinuria

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Last Updated: Apr 11, 2026

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

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Depletion of Specific Cell Populations by Complement Depletion

Depletion of Specific Cell Populations by Complement Depletion

Published on: February 5, 2010

Area of Science:

Hematology
Immunology
Complement System Biology

Background:

Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by chronic hemolytic anemia, thrombosis, and bone marrow failure.
The pathophysiology involves uncontrolled complement activation, primarily via the alternative pathway.
Deficiency of cell surface proteins CD55 and CD59 on PNH cells leads to complement-mediated cell destruction.

Purpose of the Study:

To review the role of complement activation in PNH pathogenesis.
To discuss the efficacy and limitations of current complement inhibition therapies like eculizumab.
To highlight areas of active research in complement inhibition for PNH.

Main Methods:

Literature review of PNH pathophysiology and treatment.
Analysis of complement alternative pathway involvement in hemolysis.
Evaluation of eculizumab's mechanism and clinical outcomes.

Main Results:

Eculizumab effectively inhibits terminal complement, leading to significant clinical improvement in PNH patients.
Residual complement activity persists due to upstream components and specific clinical situations.
Suboptimal responses in some patients are linked to incomplete complement blockade.

Conclusions:

Complement inhibition is a cornerstone therapy for PNH, significantly improving patient prognosis.
Further research is needed to address residual complement activity and optimize treatment strategies.
Developing novel complement inhibitors targeting upstream pathways may enhance therapeutic efficacy in PNH.