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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Properdin deficiency in a family with fulminant meningococcal infections.

Three males in a large family showed a selective deficiency of properdin ( P). One of the P deficient individuals died from a fulminant infection with Neisseria meningitidis group C. The family history revealed three previous cases of similar infections with a fatal outcome. The deficiency did not appear to be associated with repeated bacterial infections. The pattern of inheritance suggested an X-linked mode of transmittance. However, heterozygous carriers were not clearly distinguished in the family. P deficient serum supported immune haemolysis in a normal fashion. Alternative pathway functions, such as the activation of C3 by inulin or zymosan, lysis of guinea-pig erythrocytes in agarose gel and opsonization of endotoxin coated oil particles, were grossly impaired in P deficient serum while efficient C3 activation was produced by addition of cobra venom factor.[1]

References

  1. Properdin deficiency in a family with fulminant meningococcal infections. Sjöholm, A.G., Braconier, J.H., Söderström, C. Clin. Exp. Immunol. (1982) [Pubmed]
 
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