Immunostimulation by Silica Particles and the Development of Autoimmune Dysregulation

Lee, Sai Peck; Hayashi, Hiroaki; Maeda, Megumi; Matsuzaki, Naoko Kumagai-Takei Hidenori; Chen, Ying; Urakami, Kozo; MasayasuKusaka,; Nishimura, Yasumasa; Otsuki, Takemi

doi:10.5772/57544

Cited by 5 publications

(7 citation statements)

References 84 publications

(86 reference statements)

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“…30 Given that cigarette smoke contains an extremely heterogeneous mix of particulates and gases and is associated with auto-immune disease (most strongly with rheumatoid arthritis), it is biologically plausible that beyond silica, other dusts might also carry risk, consistent with our findings.…”

supporting

confidence: 85%

Prospective Risk of Rheumatologic Disease Associated with Occupational Exposure in a Cohort of Male Construction Workers

Blanc

Järvholm

Torén

2015

The American Journal of Medicine

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supporting

confidence: 85%

Prospective Risk of Rheumatologic Disease Associated with Occupational Exposure in a Cohort of Male Construction Workers

Blanc

Järvholm

Torén

2015

The American Journal of Medicine

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“…Following silica exposure, Tregs and Responder T cells (Tresps) are chronically activated and infiltrate the peripheral T cell population. By increased production of Fas ligand, Treg cells induce apoptosis and impair the immune response (97). Therefore, the overall number and inhibitory activity of T cells are reduced, with Tresps surviving due to an expression of apoptosis inhibitors (98).…”

Section: Adaptive Cellular Immune Responses In Silicosis and Tuberculmentioning

confidence: 99%

“…A significant reduction in B cells was observed in mouse spleens treated with silica nanoparticles (85). The most common effect of silica was an increase of autoantibodies such as rheumatoid factor (anti IgG), and anti-nuclear antibodies related to autoimmune diseases such as Caplan's syndrome, scleroderma, (ANCA)-related vasculitis/nephritis, and systemic lupus erythematosus (97).…”

Section: Adaptive Cellular Immune Responses In Silicosis and Tuberculmentioning

confidence: 99%

Immunity to the Dual Threat of Silica Exposure and Mycobacterium tuberculosis

et al. 2019

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Exposure to silica and the consequent development of silicosis are well-known health problems in countries with mining and other dust producing industries. Apart from its direct fibrotic effect on lung tissue, chronic and immunomodulatory character of silica causes susceptibility to tuberculosis (TB) leading to a significantly higher TB incidence in silica-exposed populations. The presence of silica particles in the lung and silicosis may facilitate initiation of tuberculous infection and progression to active TB, and exacerbate the course and outcome of TB, including prognosis and survival. However, the exact mechanisms of the involvement of silica in the pathological processes during mycobacterial infection are not yet fully understood. In this review, we focus on the host's immunological response to both silica and Mycobacterium tuberculosis, on agents of innate and adaptive immunity, and particularly on silica-induced immunological modifications in co-exposure that influence disease pathogenesis. We review what is known about the impact of silica and Mycobacterium tuberculosis or their co-exposure on the host's immune system, especially an impact that goes beyond an exclusive focus on macrophages as the first line of the defense. In both silicosis and TB, acquired immunity plays a major role in the restriction and/or elimination of pathogenic agents. Further research is needed to determine the effects of silica in adaptive immunity and in the pathogenesis of TB.

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“…One comprises T cells resistant against Fas-mediated apoptosis and now recognized as chronically activated responder T cells. The other subpopulation manifested accelerated Fas-mediated apoptosis (and was also sensitive to functional antiFas autoantibody, as described above) and is now recognized as chronically activated Treg [49,[64][65][66][67][68].…”

Section: Chronic Activation Of Regulatory T Cellsmentioning

confidence: 99%

Silica exposure and altered regulation of autoimmunity

Lee

Matsuzaki

Kumagai-Τakei

et al. 2014

Environ Health Prev Med

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Silica particles and asbestos fibers, which are known as typical causatives of pneumoconiosis, induce lung fibrosis. Moreover, silicosis patients often complicate with autoimmune diseases, and asbestos-exposed patients suffer from malignant diseases such as pleural mesothelioma and lung cancer. We have been conducting experimental studies to investigate altered regulation of selftolerance caused by silica exposure, including analyses using specimens such as plasma and immunocompetent cells obtained from silicosis patients, as a means of examining the supposition that silica exposure induces molecular and cellular biological alterations of immune cells. These approaches have resulted in the detection of several specific autoantibodies, alterations of CD95/Fas and its related molecules, and evidence of chronic activation of responder T cells and regulatory T cells following silica exposure. In this review, we present details of our investigations as an introduction to scientific approaches examining the immunological effects of environmental and occupational substances.

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Immunostimulation by Silica Particles and the Development of Autoimmune Dysregulation

Cited by 5 publications

References 84 publications

Prospective Risk of Rheumatologic Disease Associated with Occupational Exposure in a Cohort of Male Construction Workers

Prospective Risk of Rheumatologic Disease Associated with Occupational Exposure in a Cohort of Male Construction Workers

Immunity to the Dual Threat of Silica Exposure and Mycobacterium tuberculosis

Silica exposure and altered regulation of autoimmunity

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