| First Author | Medina E | Year | 1996 |
| Journal | Clin Exp Immunol | Volume | 104 |
| Issue | 1 | Pages | 44-7 |
| PubMed ID | 8603532 | Mgi Jnum | J:32074 |
| Mgi Id | MGI:79577 | Doi | 10.1046/j.1365-2249.1996.d01-656.x |
| Citation | Medina E, et al. (1996) Mice that carry the resistance allele of the Bcg gene (Bcgr) develop a superior capacity to stabilize bacille Calmette-Guerin (BCG) infection in their lungs and spleen over a protracted period in the absence of specific immunity. Clin Exp Immunol 104(1):44-7 |
| abstractText | In mice, natural resistance to infection with BCG is under the influence of an autosomal gene designated Beg. It is shown here in agreement with others that mice that possess the dominant resistant allele of the gene (Bcg(r)) are more capable than mice that possess the susceptible recessive allele (Bcg(s)) at restricting the growth of BCG in their lungs, as well as in their spleens, during the first 20 days of infection. It is shown, in addition, that in the absence of specific immunity the resistance difference between Bcg(r) and Bcg(s) mice became much more pronounced as infection progressed beyond day 20. Whereas T cell-depleted Bcg(r) mice developed a capacity after day 20 to cause infection in their lungs and spleens to stabilize and plateau for a least 40 days, T cell-depleted Bcg(s) mice were unable to prevent infection from progressing in these organs. On the other hand, both types of T cell-depleted mice were capable of causing infection to plateau in their livers and kidneys. Moreover, this T cell-independent mechanism of resistance was essentially abolished in all organs in which it was expressed by treating the mice with hydrocortisone. In the lungs of immunocompetent Bcg(s) mice, failure to stabilize infection was associated with heavily infected macrophages and failure to contain BCG at original sites of infection. |
