| First Author | Gros P | Year | 1983 |
| Journal | J Immunol | Volume | 131 |
| Issue | 4 | Pages | 1966-72 |
| PubMed ID | 6311901 | Mgi Jnum | J:7193 |
| Mgi Id | MGI:55664 | Doi | 10.4049/jimmunol.131.4.1966 |
| Citation | Gros P, et al. (1983) Cellular mechanisms of genetically controlled host resistance to Mycobacterium bovis (BCG). J Immunol 131(4):1966-72 |
| abstractText | Multiplication of Mycobacterium bovis (BCG) in the reticuloendothelial tissues of the mouse is controlled by the Chromosome 1 locus (Bcg), which exists in two allelic forms, resistant (Bcgr) and susceptible (Bcgs). We have investigated the phenotypic expression of this locus at the cellular level in vivo. No significant differences were observed in the early clearance of BCG from the bloodstream and peritoneal cavity, nor in the uptake of the infectious inoculum in spleen and liver of the mice of Bcgr and Bcgs strains. Inflammatory response to an i.p. injection of live BCG, with respect to both the cell populations involved and the kinetics of their appearance, was comparable in Bcgr and Bcgs mice. A kinetic study of BCG infection in congenitally athymic mice that carried the nude mutation on Bcgr (AKR/J) or Bcgs (BALB/c) background showed that the functional absence of T lymphocytes did not influence the expression of the Bcg gene. The population expressing the Bcg gene seems to be a mature cell of the mononuclear phagocyte lineage: it was resistant to a 950-rad dose of x-irradiation; it was susceptible to a prolonged exposure to silica; and, as demonstrated in radiation chimeras, it originated from bone marrow-derived precursors. |
