Induction of IL-17 production from human peripheral blood CD4+ cells by asbestos exposure

Maeda, Megumi; Chen, Ying; Lee, Sai Peck; Kumagai-Τakei, Naoko; Yoshitome, Kei; Matsuzaki, Hidenori; Yamamoto, Shoko; Hatayama, Tamayo; Ikeda, Miyoshi; Nishimura, Yasumasa; Otsuki, Takemi

doi:10.3892/ijo.2017.3991

Cited by 8 publications

(6 citation statements)

References 46 publications

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“…In a separate study, CD4+ lymphocytes from patients exposed to asbestos fibers exhibited altered functions of Tregs. Exposure of the CD4+ cells ex vivo showed an altered balance between Treg and Th17, with a decreased Treg response but elevated T17 response (77).…”

Section: Treg-mediated Immunosuppressive Responsementioning

confidence: 98%

“…Comparative analyses of three separate sets of microarray data obtained from mice exposed to MWCNTs implicated the Th17 response in the adverse outcome pathway (AOP) for lung fibrosis development (68). In addition, CD4+ T cells from patients exposed to asbestos showed an altered balance between Th17 and Treg responses with elevated Th17 reactions upon ex vivo exposure of the cells to chrysotile fibers (77). Therefore, exposure to inhaled particulates increases Th17 responses that are associated with altered inflammation and/or fibrosis in the lung exposed to particles.…”

Section: Th17-mediated Responsementioning

confidence: 99%

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Polarization of Immune Cells in the Pathologic Response to Inhaled Particulates

2020

Front. Immunol.

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Section: Treg-mediated Immunosuppressive Responsementioning

confidence: 98%

Section: Th17-mediated Responsementioning

confidence: 99%

Polarization of Immune Cells in the Pathologic Response to Inhaled Particulates

2020

Front. Immunol.

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“…Nonetheless, the impacts of Treg function on particle-driven inflammation remain unclear. For instance, imbalances in the Treg/Th17 ratio significantly aggravate SiO 2and MSU-induced inflammation in the lungs and joints of mice, respectively (Dai et al, 2016;Dai et al, 2018), but inhaled SiO 2 and asbestos elicit recruitment of Tregs to the lungs, which secrete TGF-β and IL-10 and contribute to resultant development of pulmonary fibrosis (Liu et al, 2010;Lo Re et al, 2011;Maeda et al, 2017). Accordingly, DCs play crucial roles in regulating T cell differentiation, interacting with proximal particles and DAMPs, and maintaining immunological self-tolerance.…”

Section: From Particle Exposure To Loss Of Immunological Self-tolerancementioning

confidence: 99%

Centrality of Myeloid-Lineage Phagocytes in Particle-Triggered Inflammation and Autoimmunity

Favor¹,

Pestka²,

Bates³

et al. 2021

Front. Toxicol.

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Exposure to exogenous particles found as airborne contaminants or endogenous particles that form by crystallization of certain nutrients can activate inflammatory pathways and potentially accelerate autoimmunity onset and progression in genetically predisposed individuals. The first line of innate immunological defense against particles are myeloid-lineage phagocytes, namely macrophages and neutrophils, which recognize/internalize the particles, release inflammatory mediators, undergo programmed/unprogrammed death, and recruit/activate other leukocytes to clear the particles and resolve inflammation. However, immunogenic cell death and release of damage-associated molecules, collectively referred to as “danger signals,” coupled with failure to efficiently clear dead/dying cells, can elicit unresolved inflammation, accumulation of self-antigens, and adaptive leukocyte recruitment/activation. Collectively, these events can promote loss of immunological self-tolerance and onset/progression of autoimmunity. This review discusses critical molecular mechanisms by which exogenous particles (i.e., silica, asbestos, carbon nanotubes, titanium dioxide, aluminum-containing salts) and endogenous particles (i.e., monosodium urate, cholesterol crystals, calcium-containing salts) may promote unresolved inflammation and autoimmunity by inducing toxic responses in myeloid-lineage phagocytes with emphases on inflammasome activation and necrotic and programmed cell death pathways. A prototypical example is occupational exposure to respirable crystalline silica, which is etiologically linked to systemic lupus erythematosus (SLE) and other human autoimmune diseases. Importantly, airway instillation of SLE-prone mice with crystalline silica elicits severe pulmonary pathology involving accumulation of particle-laden alveolar macrophages, dying and dead cells, nuclear and cytoplasmic debris, and neutrophilic inflammation that drive cytokine, chemokine, and interferon-regulated gene expression. Silica-induced immunogenic cell death and danger signal release triggers accumulation of T and B cells, along with IgG-secreting plasma cells, indicative of ectopic lymphoid tissue neogenesis, and broad-spectrum autoantibody production in the lung. These events drive early autoimmunity onset and accelerate end-stage autoimmune glomerulonephritis. Intriguingly, dietary supplementation with ω-3 fatty acids have been demonstrated to be an intervention against silica-triggered murine autoimmunity. Taken together, further insight into how particles drive immunogenic cell death and danger signaling in myeloid-lineage phagocytes and how these responses are influenced by the genome will be essential for identification of novel interventions for preventing and treating inflammatory and autoimmune diseases associated with these agents.

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“…IL-17 signaling in colorectal carcinoma promotes tumorigenesis by preventing the production of T cell-attracting CXCL9 and CXCL10 in tumor cells (46). Interestingly, asbestos exposure increases IL-17 production, especially in CD4+ surface CXCR3+ cells, indicating that the relation between Treg and Th17 fractions is important for asbestos immunogenicity and decrease in anti-tumor immunity (47). This is in accordance with the findings of Zebedeo et al, who found increased production of IL-17, IL-6, TGF-β, and TNF-α in mice following exposure to erionite and amphibole asbestos (48).…”

Section: Interleukin-17 (Il-17)mentioning

confidence: 99%

Mitogen signal-associated pathways, energy metabolism regulation, and mediation of tumor immunogenicity play essential roles in the cellular response of malignant pleural mesotheliomas to platinum-based treatment: a retrospective study

Mathilakathu¹,

Borchert²,

Wessolly³

et al. 2021

Transl Lung Cancer Res

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Background: Malignant pleural mesothelioma (MPM) is a rare malignant tumor associated with asbestos exposure, with infaust prognosis and overall survival below 20 months in treated patients. Platinum is still the backbone of the chemotherapy protocols, and the reasons for the rather poor efficacy of platinum compounds in MPM remain largely unknown. Therefore, we aimed to analyze differences in key signaling pathways and biological mechanisms in therapy-naïve samples and samples after chemotherapy in order to evaluate the effect of platinum-based chemotherapy.Methods: The study cohort comprised 24 MPM tumor specimens, 12 from therapy-naïve and 12 from patients after platinum-based therapy. Tumor samples were screened using the NanoString nCounter platform for digital gene expression analysis with an appurtenant custom-designed panel comprising a total of 366 mRNAs covering the most important tumor signaling pathways. Significant pathway associations were identified by gene set enrichment analysis using the WEB-based GEne SeT AnaLysis Toolkit (WebGestalt)Results: We have found reduced activity of TNF (normalized enrichment score: 2.03), IL-17 (normalized enrichment score: 1.93), MAPK (normalized enrichment score: 1.51), and relaxin signaling pathways (normalized enrichment score: 1.42) in the samples obtained after platinum-based therapy. In contrast, AMPK (normalized enrichment score: -1.58), mTOR (normalized enrichment score: -1.50), Wnt (normalized enrichment score: -1.38), and longevity regulating pathway (normalized enrichment score: -1.31) showed significantly elevated expression in the same samples. Conclusion:We could identify deregulated signaling pathways due to a directed cellular response to platinum-induced cell stress. Our results are paving the ground for a better understanding of cellular responses and escape mechanisms, carrying a high potential for improved clinical management of patients with MPM.

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Induction of IL-17 production from human peripheral blood CD4+ cells by asbestos exposure

Cited by 8 publications

References 46 publications

Polarization of Immune Cells in the Pathologic Response to Inhaled Particulates

Polarization of Immune Cells in the Pathologic Response to Inhaled Particulates

Centrality of Myeloid-Lineage Phagocytes in Particle-Triggered Inflammation and Autoimmunity

Mitogen signal-associated pathways, energy metabolism regulation, and mediation of tumor immunogenicity play essential roles in the cellular response of malignant pleural mesotheliomas to platinum-based treatment: a retrospective study

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