The human immune response to tuberculosis and its treatment: a view from the blood.
Bottom Line: Using modular and pathway analyses of the complex data has shown, now in multiple studies, that the signature of active tuberculosis is dominated by overexpression of interferon-inducible genes (consisting of both type I and type II interferon signaling), myeloid genes, and inflammatory genes.There is also downregulation of genes encoding B and T-cell function.The signature suggested a previously under-appreciated role for type I interferons in development of active tuberculosis disease, and numerous mechanisms have now been uncovered to explain how type I interferon impedes the protective response to M. tuberculosis infection.
Affiliation: TB Centre and Department of Immunology and Infection, London School of Hygiene & Tropical Medicine, London, UK.Show MeSH
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Mentions: Transcriptomic analyses of blood from patients with tuberculosis has revealed a dominant signature of IFN-inducible genes, including those down-stream of type I and type II (IFN-γ) signaling (4, 8, 10, 12), upregulation of complement related genes (12) and those associated with myeloid function and inflammation (4, 7, 8, 11, 12, 21, 62) (Fig.6). In addition, the signature reflects downregulation of genes encoding B and T-cell functions (4, 12, 21) (Fig.6), the latter accounted for by decreased numbers of T cells in the blood of active tuberculosis patients (4). This perhaps reflects apoptosis of such cells in the blood or their migration to the infected tissue (4).
Affiliation: TB Centre and Department of Immunology and Infection, London School of Hygiene & Tropical Medicine, London, UK.