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C5 DEFICIENCY IN A/J MICE IS NOT ASSOCIATED WITH RESISTANCE TO THE DEVELOPMENT OF SECONDARY AMYLOIDOSIS
Author(s) -
Coutinho M.,
Zahedi K.,
Whitehead A. S.,
Davis A. E.
Publication year - 1992
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/j.1744-313x.1992.tb00085.x
Subject(s) - amyloidosis , hindiii , amyloid (mycology) , heterozygote advantage , biology , aa amyloidosis , pathology , immunology , microbiology and biotechnology , endocrinology , genotype , dna , medicine , genetics , restriction enzyme , disease , gene , familial mediterranean fever
SUMMARY The aim of the study was to determine whether C5 deficiency in the mouse is associated with resistance to the development of secondary amyloidosis. Chronic inflammation was induced in the F 2 progeny, derived from matings between amyloid‐susceptible and amyloid‐resistance mice, by daily injections of azocasein for thirty days. Using a restriction fragment length polymorphism generated by digestion of genomic DNA with the restriction enzyme HindIII, C5 sufficient and deficient DNA can be clearly differentiated. Eight mice were found to be C5 sufficient, 32 were heterozygotes and 14 were found to be C5 deficient. Grading of the splenic amyloid load from negative to 4+ was performed after staining tissue squashes with Congo red and viewing them under a polarizing microscope. Seventeen mice were noted to have negative to trace, 18 had moderate (1+‐2+) and 19 had heavy (3 H+‐4+) amyloid deposition. There was no correlation between splenic amyloid load and C5 deficiency. Based on these results it is clear that C5 deficiency and resistance to secondary amyloidosis are not associated.