Abstract
Blood transcriptomics analysis of tuberculosis has revealed an interferon-inducible gene signature that diminishes in expression after successful treatment; this promises improved diagnostics and treatment monitoring, which are essential for the eradication of tuberculosis. Sensitive radiography revealing lung abnormalities and blood transcriptomics have demonstrated heterogeneity in patients with active tuberculosis and exposed asymptomatic people with latent tuberculosis, suggestive of a continuum of infection and immune states. Here we describe the immune response to infection with Mycobacterium tuberculosis revealed through the use of transcriptomics, as well as differences among clinical phenotypes of infection that might provide information on temporal changes in host immunity associated with evolving infection. We also review the diverse blood transcriptional signatures, composed of small sets of genes, that have been proposed for the diagnosis of tuberculosis and the identification of at-risk asymptomatic people and suggest novel approaches for the development of such biomarkers for clinical use.
Highlights
Blood transcriptomics in tuberculosis have revealed an IFN-inducible signature that diminished upon successful treatment, promising improved diagnostics and treatment monitoring, essential to eradicate tuberculosis
Current diagnosis for latent TB infection (LTBI), involves testing reactivity to mycobacterial antigens, determined by a tuberculin skin test (TST), or an M. tuberculosis-specific interferon-γ (IFN-γ) release assay (IGRA), which can demonstrate whether a T cell mediated immune response has been elicited in response to the infection[6], but both tests have poor prognostic value
Protective factors have been described, including IL-12, IFN-γ and TNF-α, our understanding of the early phase of M. tuberculosis infection or progression to disease in humans is very limited 2,10–13,14,15
Summary
Author manuscript; available in PMC 2019 June 06. Published in final edited form as: Nat Immunol. Akul Singhania[1], Robert J. Wilkinson[2,3,4], Marc Rodrigue[5], Pranabashis Haldar[6], and Anne O’Garra1,7 1Laboratory of Immunoregulation and Infection, The Francis Crick Institute, London NW1 1AT, United Kingdom 2Laboratory of Tuberculosis, The Francis Crick Institute, London NW1 1AT, United Kingdom 3Department of Medicine, Imperial College London, London W2 1PG, United Kingdom 4Wellcome Centre for Infectious Diseases Research in Africa, University of Cape Town, Observatory 7925, Republic of South Africa 5Medical Diagnostic Discovery Department, bioMérieux SA, 69280 Marcy l’Etoile, France 6Respiratory Biomedical Research Centre, Institute for Lung Health, Department of Infection Immunity and Inflammation, University of Leicester, Leicester LE3 9QP, United Kingdom 7National Heart and Lung Institute, Imperial College London, London W2 1PG, United Kingdom
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