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- Publisher
- Wolters Kluwer Health
- ISSN
- 1746-630X
- eISSN
- 1746-6318
- DOI
- 10.1097/COH.0000000000000501
- Publisher site
- See Article on Publisher Site
Abstract
Downloaded from http://journals.lww.com/co-hivandaids by BhDMf5ePHKbH4TTImqenVA5KvPVPZ0P5BEgU+IUTEfzO/GUWifn2IfwcEVVH9SSn on 06/02/2020 REVIEW URRENT Recent progress in understanding immune PINION activation in the pathogenesis in HIV–tuberculosis co-infection a, a,b, a,c a,d Elsa du Bruyn , Nashied Peton , Hanif Esmail , Patrick J. Howlett , a,b,e,f a,d,g Anna K. Coussens , and Robert J. Wilkinson Purpose of review Tuberculosis is the leading infectious cause of death worldwide, and HIV-1 the best recognized risk factor for active TB. This review focuses on immune complex formation; the interplay of type I and II interferon signaling; and T-cell activation in HIV–TB pathogenesis. Recent findings Circulating immune complexes and complement, and Fcg signaling in whole blood act as early markers of TB disease in HIV-1-infected persons. HIV-1 is associated with a type I interferon response in whole blood, reducing the specificity of TB biomarkers dependent on type I and II interferon genes. Type I and type II interferons are implicated in both protection and TB disease, a protective outcome may depend on modulating these pathways. Whilst M. tuberculosis-specific CD4 T cells are preferentially depleted during HIV-1 infection, activation markers on M. tuberculosis-specific CD4 T cells, in particular HLA-DR, reflect immune activation and have promise as biomarkers of M.
Journal
Current Opinion in HIV & AIDS – Wolters Kluwer Health
Published: Nov 1, 2018