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Identification of complement factor 5 as a susceptibility locus for experimental allergic asthma
1Department of Medicine, Johns Hopkins University, School of Medicine, Baltimore, MA, USA. mkarp@wekh.jhu.edu
Nature Immunology
|March 23, 2001
Summary
Complement factor 5 (C5) gene variations increase susceptibility to allergic asthma. C5 deficiency impairs interleukin-12 (IL-12) production, a key factor in asthma development and regulation.
Area of Science:
- Immunology
- Genetics
- Pulmonology
Background:
- Allergic asthma prevalence and severity are increasing globally.
- Identifying environmental triggers and genetic factors is crucial for understanding asthma pathogenesis.
Purpose of the Study:
- To identify genetic susceptibility loci for allergen-induced airway hyperresponsiveness.
- To elucidate the role of complement factor 5 (C5) in asthma development.
Main Methods:
- Microarray analysis of pulmonary gene expression.
- Single nucleotide polymorphism (SNP)-based genotyping.
- Quantitative trait locus (QTL) analysis in a murine asthma model.
Main Results:
- The gene encoding complement factor 5 (C5) was identified as a susceptibility locus for allergic asthma.
- A deletion in the C5 coding sequence resulted in C5-deficiency and increased asthma susceptibility.
- Blockade of the C5a receptor inhibited IL-12 production in human monocytes, similar to C5-deficient mice.
Conclusions:
- Complement factor 5 (C5) plays a significant role in regulating susceptibility to allergic asthma.
- C5 influences asthma pathogenesis by modulating interleukin-12 (IL-12) production.
- Immunoregulatory events involving complement are critical at the innate-adaptive immunity interface in asthma.
