Virulence of a Mycobacterium tuberculosis clinical isolate in mice is determined by failure to induce Th1 type immunity and is associated with induction of IFN-α/β

By C. Manca, L. Tsenova, A. Bergtold, S. Freeman, Micah Tovey, J. Musser, C. Barry, V. Freedman, G. Kaplan. Proceedings of the National Academy of Sciences of the United States of America, 2001

654 citations recorded by the source corpus.

Subfields: Epidemiology, Infectious Diseases, Oncology

View Paper: https://www.semanticscholar.org/paper/c7e4d84937550b2d0195802605246c04fd80892b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. A. O’Garra
2. R. Wilkinson
3. I. Smith
4. G. Trinchieri
5. M. Berry
6. Finlay W Mcnab
7. Paul S. Redford
8. C. Bloom

In Infectious Diseases

1. A. O’Garra
2. R. Wilkinson
3. I. Smith
4. G. Trinchieri
5. M. Berry
6. Finlay W Mcnab
7. Paul S. Redford
8. C. Bloom

Citations in the corpus

• Mycobacterium tuberculosis Pathogenesis and Molecular Determinants of Virulence (2003, background): “tuberculosis clinical strains are more virulent than others (178).”
• Type I interferon: friend or foe? (2010, background): “Furthermore, the ability of Mycobacterium tuberculosis strains to induce type I IFN production has been proposed to correlate with bacterial virulence (Manca et al., 2001, 2005).”
• The immune response in tuberculosis. (2013, background): “tuberculosis isolates, CDC1551 and HN878 [previously shown to differ in virulence and immunogenicity in mouse and rabbit models of TB (24, 335) but to grow with similar rates], induced transcription of distinct sets of genes (337).”
• ISG15 in antiviral immunity and beyond (2018, background): “As an increase in type I interferon signalling has been correlated with an increased severity of mycobacterial infections 124, 125 , it is likely that both mechanisms contribute to the observed increased susceptibility.”