Previous studies have shown that C57L and DBA/2 mice are able to control the initial net growth of Salmonella typhimurium in splenic and hepatic tissues, but when infected i.p., they ultimately succumb to the typhoid-like disease caused by this Gram-negative bacterium. In this investigation, it was observed that the late-phase susceptibility of both the C57L and DBA/2 strains to murine typhoid was not only evident when mice were challenged i.p., but also when mice were challenged subcutaneously, i.v., and orally. Genetic analyses were then performed to characterize the gene or genes responsible for this susceptibility. The results of such experiments were consistent with the hypothesis that a single autosomal recessive gene is primarily responsible for the susceptibility. This gene was distinct from all other previously defined S. typhimurium response genes. The chromosomal location of the late-phase susceptibility gene could not be determined; no linkage was observed between expression of the late-phase susceptible phenotype and selected markers on chromosomes 1, 2, 4, 5, or 7.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Immunology|
|State||Published - 1984|
ASJC Scopus subject areas
- Immunology and Allergy