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- W2097410798 abstract "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." @default.
- W2097410798 created "2016-06-24" @default.
- W2097410798 creator A5024307673 @default.
- W2097410798 creator A5025525839 @default.
- W2097410798 date "2003-09-15" @default.
- W2097410798 modified "2023-10-01" @default.
- W2097410798 title "Reactivation of Latent Tuberculosis Infection in TNF-Deficient Mice" @default.
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- W2097410798 doi "https://doi.org/10.4049/jimmunol.171.6.3110" @default.
- W2097410798 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12960337" @default.
- W2097410798 hasPublicationYear "2003" @default.
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