Table 1.
Summary of mechanisms associated with IL-17 activity, and how these impact outcomes in TB.
Fig 1.
Dual role of IL-17 responses and associated clinical outcomes at different stages of TB.
Protective role of Th17 – IL-17 in the early stages of Mtb infection (blue/left) and detrimental effects in the context of symptomatic active disease (red/right), and the IL-17-mediated mechanisms associated with these outcomes. Below, the drivers of IL-17 induction and the functional consequences of the ensuing IL-17 signalling activity: (1) dendritic cells (DCs) and macrophages (Mϕ) immune activation by Mtb, (2) release of IL-23, IL-1β, IL-6 and TGF-β to differentiate Th17 cells from naïve T cells (T0), CD40 expression on DCs is central to enhance Th17 polarisation, (3) release of IL-17 and IL-22 by activated Th17, which (4) triggers release of neutrophil chemokines and antimicrobial peptides from epithelial cells and alveolar macrophages that may control Mtb replication. (5) Neutrophils recruited to the site of infection contribute to ROS production which may be protective, but in established disease may also contribute to (6) induction of matrix metalloproteases that promote tissue damage. Figure generated using BioRender. Maseeme, M. (2026) https://BioRender.com/anzbb6v.