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Related Experiment Video

Updated: Jun 25, 2026

Depletion of Specific Cell Populations by Complement Depletion

Depletion of Specific Cell Populations by Complement Depletion

Published on: February 5, 2010

The spectrum of complement alternative pathway-mediated diseases.

V Michael Holers¹

¹Department of Medicine and Immunology, University of Colorado Denver School of Medicine, Aurora, CO 80045, USA. michael.holers@uchsc.edu

Immunological Reviews

|July 11, 2008

Summary

The complement system, particularly its alternative pathway, is a key target for treating inflammatory and autoimmune diseases. Therapies inhibiting this pathway show promise in reducing tissue injury and disease severity.

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Area of Science:

Immunology
Molecular Biology
Therapeutic Development

Background:

The complement system is crucial in immune responses and inflammation.
Recent therapeutic advancements highlight complement as a viable drug target.
The alternative pathway plays a significant role in various disease models.

Purpose of the Study:

To review the evidence supporting the alternative pathway's role in tissue injury.
To explore the rationale for developing therapies targeting the alternative pathway.
To discuss the complexity of modulating complement activation.

Main Methods:

Review of preclinical studies using animal models and human samples.
Analysis of genetic data from human diseases associated with complement dysregulation.
Examination of therapeutic strategies targeting complement component C5.

Main Results:

Inhibition of complement component C5 with eculizumab is effective for paroxysmal nocturnal hemoglobinuria.
Alternative pathway activation is implicated in atypical hemolytic uremic syndrome, dense deposit disease, and age-related macular degeneration.
Complement inhibition demonstrates potential in ameliorating inflammatory and autoimmune disease manifestations.

Conclusions:

The alternative pathway is essential in mediating tissue injury.
Targeting the alternative pathway offers a promising therapeutic strategy for inflammatory and autoimmune diseases.
Further research is needed to optimize cost-effective complement inhibition therapies.