Abstract
In tuberculosis (TB), protective inflammatory immune responses and the pathological sequelae of chronic inflammation significantly depend on a timely balance of cytokine expression. In contrast to other anti-inflammatory cytokines, interleukin (IL)-27 has fundamental effects in experimental Mycobacterium tuberculosis (Mtb) infection: the absence of IL-27-mediated signalling promotes a better control of mycobacterial growth on the one hand side but also leads to a chronic hyperinflammation and immunopathology later during infection. Hence, in the context of novel host-directed therapeutic approaches and vaccination strategies for the management of TB, the timely restricted blockade of IL-27 signalling may represent an advanced treatment option. In contrast, administration of IL-27 itself may allow to treat the immunopathological consequences of chronic TB. In both cases, a better knowledge of the cell type-specific and kinetic effects of IL-27 after Mtb infection is essential. This review summarizes IL-27-mediated mechanisms affecting protection and immunopathology in TB and discusses possible therapeutic applications.
Highlights
Tuberculosis (TB) is an infectious bacterial disease caused by Mycobacterium tuberculosis (Mtb) that has challenged humanity for millennia [1]
In vivo mouse data provide a comprehensive picture of the IL27-mediated effects on the structure of lung granulomas as well as on the localization and intrinsic quality of effector CD4+ T cell subsets during Mtb infection [30, 67]
Initial findings from in vivo and in vitro studies indicate that the pleiotropic cytokine IL-27 may affect other innate and adaptive immune subsets during TB [30, 48, 96,97,98]
Summary
Tuberculosis (TB) is an infectious bacterial disease caused by Mycobacterium tuberculosis (Mtb) that has challenged humanity for millennia [1]. In the absence of IL-27Ra, higher numbers of CD8+ T cells accumulate in the lungs of Mtb-infected mice [48] (Figure 2, Table 1) These CD8+ T cells exhibit enhanced expression of activation markers. Activated lung CD8+ T cells may be a part of the improved antimycobacterial immunity in IL-27Ra-/- mice, eventually resulting in a more efficient containment of Mtb. As mentioned before, in the absence of IL-27Ra, Mtbinfected lungs exhibit highly structured granulomas surrounded by a lymphocyte rim which predominantly contains clusters of B cells - an effect that is strikingly dependent on the expression of IL-17A [30] Antigen presenting cells (APC), such as MF and DC, are able to initiate granuloma formation and adaptive immunity by the presentation of antigen and the secretion of pro-inflammatory
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