Summary
Selective breedings of mice were carried out for quantitative antibody responsiveness to flagellar Ag., f (Selection III) or somatic Ag., s (Selection IV) of two non cross‐reaction Salmonellae (Salm. tm., Salm. or.) alternated for immunization of consecutive generations. At the selection limit, these selections produced homozygous high (H) and low (L) responder lines for the character investigated: peak agglutinin response to optimal secondary immunization. The responsiveness to both f and s Ags. is submitted to polygenic regulation. The heritability (h2) realized during the selective breeding was 0.37 ± 0.07 for the response to f Ag. and 0.40 ± 0.1 for the response to s Ag. The respective part of genetic and environmental variance in F2 hybrids was 64% and 36% in selection III and 61% and 39% in selection IV. In the two selections, the dominance variance is negligible (<1%), therefore the genetic variance is essentially additive. The additive variance calculated as the heritable fraction of the F2 hybrid variance is somewhat lower, the reason for this difference is discussed. The quantitative antibody response to f Ag. in selection III is controlled by about seven independent loci. The antibody response to s Ag. in selection IV is controlled by about four independent loci. A possible association of relevant genes with the H‐2 locus was investigated. In selection III, no significant participation of H‐2 linked genes, in the regulation of responses to f and s Ags. of Salm, tm and Salm. or. could be demonstrated. In selection IV a partial contribution of H‐2 linked genes was observed concerning responsiveness to both f and s Ags. of Salm. tm.. but not to Salm. or. Ags. The H‐2 effect accounts for 25% of the total interline difference.
The genetically selected high antibody responder mice (HIII) are susceptible and the low antibody responder mice (LIII) are resistant to the experimental infection with Mouse Hepatitis Virus 3 (MHV3). The mortality rates of the F1 hybrids and of the F2 segregants showed the codominance of the susceptible and resistant characters. The direct individual intrapopulation correlation between the induction of antiviral state in macrophages activated by IFN gamma and the resistance to the virus infection, showed that an antiviral state could be induced in resistant mouse macrophages, whereas in susceptible mouse macrophages no restriction of virus replication could be observed. A direct inter- and intrapopulation correlation of pre-existing antibody titres against MHV3 with the mortality and a direct interpopulation correlation of those titres with the mean survival time of susceptible animals was shown. The data indicate, among the mechanisms of resistance against the virus infection, a role of IFN gamma macrophage-activation and of antibodies against MHV3 which may delay the mean survival time in susceptible animals.
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