| First Author | Botha T | Year | 2003 |
| Journal | J Immunol | Volume | 171 |
| Issue | 6 | Pages | 3110-8 |
| PubMed ID | 12960337 | Mgi Jnum | J:85390 |
| Mgi Id | MGI:2674215 | Doi | 10.4049/jimmunol.171.6.3110 |
| Citation | Botha T, et al. (2003) Reactivation of latent tuberculosis infection in TNF-deficient mice. J Immunol 171(6):3110-8 |
| abstractText | TNF-deficient mice are highly susceptible to Mycobacterium tuberculosis H37Rv infection. Here we asked whether TNF is required for postinfectious immunity in aerosol-infected mice. Chemotherapy for 4 wk commencing 2 wk postinfection reduced CFU to undetectable levels. While wild-type mice had a slight rise in CFU, but controlled infection upon cessation of chemotherapy, TNF-deficient mice developed reactivation of infection with high bacterial loads in lungs, spleen, and liver, which was fatal within 13-18 wk. The increased susceptibility of TNF-deficient mice was accompanied by diminished recruitment and activation of T cells and macrophages into the lung, with defective granuloma formation and reduced inducible NO synthase expression. Reduced chemokine production in the lung might explain suboptimal recruitment and activation of T cells and uncontrolled infection. Therefore, despite a massive reduction of the mycobacterial load by chemotherapy, TNF-deficient mice were unable to compensate and mount a protective immune response. In conclusion, endogenous TNF is critical to maintain latent tuberculosis infection, and in its absence no specific immunity is generated. |
