<i>Mycobacterium tuberculosis</i> multi-drug-resistant strain M induces IL-17+IFNγ– CD4+ T cell expansion through an IL-23 and TGF-β-dependent mechanism in patients with MDR-TB tuberculosis

Basile, Juan I.; Kviatcovsky, Denise; Romero, M. Carolina; Balboa, Luciana; Monteserin, Johana; Ritacco, Viviana; López, Beatriz; García, Carolina Carrizo; Garcı́a, Ana Maria; Vescovo, Marisa; Montaner, Pablo González; Palmero, Domingo; Sasiain, Marı́a del Carmen; Barrera, Silvia de la

doi:10.1111/cei.12873

Cited by 24 publications

(28 citation statements)

References 48 publications

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“…These results were in line with other studies performed with lipopolysaccharide-activated human MoDCs where IL-23 neutralization provoked a decrease in IL-17A production from allogeneic CD4 þ T cells (Roses et al, 2008). Human DC-derived IL-23 is also a key factor in IL-17A production by T cells in response to pathogens such as Candida albicans (Maher et al, 2015), Mycobacterium tuberculosis (Basile et al, 2017), and other bacteria (van Beelen et al, 2007) acting through TLR2/4 and NOD2 signaling pathways.…”

Section: Discussionsupporting

confidence: 91%

Nickel Sulfate Promotes IL-17A Producing CD4+ T Cells by an IL-23-Dependent Mechanism Regulated by TLR4 and Jak-STAT Pathways

Bechara

Antonios

Azouri

et al. 2017

Journal of Investigative Dermatology

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Allergic contact dermatitis, caused by nickel, is a delayed-type hypersensitivity reaction, and 14.5% of the general population may be affected in Europe. Among a wide range of cytokines, the IL-12 family has unique structural and immunological characteristics. Whereas IL-12p70 promotes T helper (Th) 1 cell polarization, IL-23 promotes Th17 cell development and both have been isolated from nickel-allergic patients. In this work, we were interested in understanding the mechanism behind nickel-induced Th17 cell development. We showed that nickel induced an early production of IL-23 in human monocyte-derived dendritic cells along with an increase in the expression of il-23p19 and il-12p40 mRNA. However, the production of a significant level of IL-12p70 required an additional signal such as IFN-γ. Moreover, nickel-treated monocyte-derived dendritic cells induced an increase in the percentage of IL-17A CD4 T cells, an effect reduced by IL-23 neutralization. We then investigated the molecular mechanism of IL-23 production. Our results showed that toll-like receptor 4, p38 mitogen-activated protein kinase, and NF-κB were involved in IL-23 production induced by nickel. However, Jak-signal transducer and activator of transcription activation seems to maintain the IL-23/IL-12p70 balance by limiting IL-23 production and promoting Th1 polarization. These results indicate that nickel-induced Th17 cell development is dependent on the production of IL-23 by human monocyte-derived dendritic cells via toll-like receptor 4, p38 mitogen-activated protein kinase, NF-κB, and Jak-signal transducer and activator of transcription pathways.

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Section: Discussionsupporting

confidence: 91%

Nickel Sulfate Promotes IL-17A Producing CD4+ T Cells by an IL-23-Dependent Mechanism Regulated by TLR4 and Jak-STAT Pathways

Bechara

Antonios

Azouri

et al. 2017

Journal of Investigative Dermatology

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“…Transforming growth factor-β TGF-β belongs to the TGF superfamily produced by all white blood cell lineages. 84 Costimulation of TGF-β with IL-6 is required for Th17 cell differentiation. 85 The TGF-β1 content in the serum of TB patients is higher than that in HC controls, and the serum level of TGF-β1 is directly related to the bacterial load and radiological severity.…”

Section: Mtb Infection Regulates the Expression Of Upstream Cytokinesmentioning

confidence: 99%

The crucial roles of Th17-related cytokines/signal pathways in M. tuberculosis infection

2017

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Interleukin-17 (IL-17), IL-21, IL-22 and IL-23 can be grouped as T helper 17 (Th17)-related cytokines because they are either produced by Th17/Th22 cells or involved in their development. Here, we review Th17-related cytokines/Th17-like cells, networks/signals and their roles in immune responses or immunity against Mycobacterium tuberculosis (Mtb) infection. Published studies suggest that Th17-related cytokine pathways may be manipulated by Mtb microorganisms for their survival benefits in primary tuberculosis (TB). In addition, there is evidence that immune responses of the signal transducer and activator of transcription 3 (STAT3) signal pathway and Th17-like T-cell subsets are dysregulated or destroyed in patients with TB. Furthermore, Mtb infection can impact upstream cytokines in the STAT3 pathway of Th17-like responses. Based on these findings, we discuss the need for future studies and the rationale for targeting Th17-related cytokines/signals as a potential adjunctive treatment.

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Section: Interactions Between T1-ifns and Th17 Immunity In Tbmentioning

confidence: 99%

“…With regard to the role of IL-1β and IL-23 in human TB, IL-1β is essential for the expansion of both IFN-γ − IL-17 + Th17 cells and IFN-γ + IL-17 + Th17 cells (311, 312). IL-23 promotes the development of IFN-γ + IL-17 + Th17 cells but promotes IFN-γ − IL-17 + Th17 cells if TGF-β is concomitantly present (312). Since active TB is associated with elevated TGF-β levels (178, 313, 314), it is possible that Th17.1 cell differentiation does not play a major role, but this remains to be demonstrated.…”

Section: Interactions Between T1-ifns and Th17 Immunity In Tbmentioning

confidence: 99%

Interactions between Type 1 Interferons and the Th17 Response in Tuberculosis: Lessons Learned from Autoimmune Diseases

et al. 2017

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The classical paradigm of tuberculosis (TB) immunity, with a central protective role for Th1 responses and IFN-γ-stimulated cellular responses, has been challenged by unsatisfactory results of vaccine strategies aimed at enhancing Th1 immunity. Moreover, preclinical TB models have shown that increasing IFN-γ responses in the lungs is more damaging to the host than to the pathogen. Type 1 interferon signaling and altered Th17 responses have also been associated with active TB, but their functional roles in TB pathogenesis remain to be established. These two host responses have been studied in more detail in autoimmune diseases (AID) and show functional interactions that are of potential interest in TB immunity. In this review, we first identify the role of type 1 interferons and Th17 immunity in TB, followed by an overview of interactions between these responses observed in systemic AID. We discuss (i) the effects of GM-CSF-secreting Th17.1 cells and type 1 interferons on CCR2+ monocytes; (ii) convergence of IL-17 and type 1 interferon signaling on stimulating B-cell activating factor production and the central role of neutrophils in this process; and (iii) synergy between IL-17 and type 1 interferons in the generation and function of tertiary lymphoid structures and the associated follicular helper T-cell responses. Evaluation of these autoimmune-related pathways in TB pathogenesis provides a new perspective on recent developments in TB research.

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Mycobacterium tuberculosis multi-drug-resistant strain M induces IL-17+IFNγ– CD4+ T cell expansion through an IL-23 and TGF-β-dependent mechanism in patients with MDR-TB tuberculosis

Cited by 24 publications

References 48 publications

Nickel Sulfate Promotes IL-17A Producing CD4+ T Cells by an IL-23-Dependent Mechanism Regulated by TLR4 and Jak-STAT Pathways

Nickel Sulfate Promotes IL-17A Producing CD4+ T Cells by an IL-23-Dependent Mechanism Regulated by TLR4 and Jak-STAT Pathways

The crucial roles of Th17-related cytokines/signal pathways in M. tuberculosis infection

Interactions between Type 1 Interferons and the Th17 Response in Tuberculosis: Lessons Learned from Autoimmune Diseases

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