| First Author | Kobayashi K | Year | 1996 |
| Journal | J Infect Dis | Volume | 174 |
| Issue | 3 | Pages | 564-73 |
| PubMed ID | 8769615 | Mgi Jnum | J:35038 |
| Mgi Id | MGI:82489 | Doi | 10.1093/infdis/174.3.564 |
| Citation | Kobayashi K, et al. (1996) Interleukin (IL)-12 deficiency in susceptible mice infected with Mycobacterium avium and amelioration of established infection by IL-12 replacement therapy. J Infect Dis 174(3):564-73 |
| abstractText | Mycobacterium avium is an intracellular microorganism that infects and multiplies within macrophages. Cell-mediated immunity plays an important role in host defense, and interleukin (IL)-12, which is produced mainly by macrophages, is critical for its development. In a mouse model of disseminated M. avium infection, genetically susceptible BALB/c mice had increased mycobacterial growth and decreased IL-12 expression and developed large and numerous granulomas. In contrast, resistant DBA/2 mice exhibited reduced mycobacterial burden with increased IL-12 expression and developed fewer and smaller granulomas. In susceptible mice with established M. avium infection, IL-12 replacement therapy resulted in persistent reduction of mycobacterial burdens. IL-12 itself, however, could not inhibit mycobacterial growth in vitro. By enhancing host defenses, IL-12 exerts a potent mycobactericidal activity in vivo with low toxicity. This suggests that IL-12 replacement therapy is rational for M. avium infection in susceptible hosts. |
