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Complement C7 M/N allotyping in infectious diseases

R Würzner¹, B M Sölder, W M Prodinger

¹Institute for Hygiene, University of Innsbruck, Austria.

Experimental and Clinical Immunogenetics

|January 1, 1995

Summary

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This study investigated the C7 M/N polymorphism in 528 patients, finding no significant disease associations for the C7*M or C7*N alleles. The hypothesis linking Lyme borreliosis to the C7*N allele was specifically refuted.

Area of Science:

Immunogenetics
Complement System Biology
Molecular Diagnostics

Background:

The C7 M/N polymorphism represents a variation in the seventh component of complement (C7).
Understanding the association between complement allotypes and diseases is crucial for diagnostics and treatment.

Purpose of the Study:

To investigate potential disease associations of the C7*M and C7*N alleles.
To test the hypothesis that the hypomorphic C7*N allele is associated with an increased frequency of Lyme borreliosis.

Main Methods:

Enzyme-Linked Immunosorbent Assay (ELISA) was employed to determine C7 M/N allotypes.
The reactivity of the allospecific monoclonal antibody WU 4-15 was compared with polyclonal anti-C7 IgG.
A cohort of 528 hospitalized patients, primarily with infectious diseases, was analyzed.

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Main Results:

No statistically significant association was found between either the C7*M or C7*N alleles and any specific disease.
The study specifically refuted the hypothesis that homozygous carriers of the C7*N allele are more prone to Lyme borreliosis.

Conclusions:

The C7 M/N polymorphism does not appear to be a significant risk factor for the infectious diseases studied.
The findings exclude a specific role for the C7*N allele in the susceptibility to Lyme borreliosis.