Induction of CD69 antigen expression in peripheral blood mononuclear cells on exposure to silica, but not by asbestos/chrysotile-A

Wu, Ping; Hyodoh, Fuminori; Hatayama, Tamayo; Sakaguchi, Haruko; Hatada, Satomi; Miura, Yoshie; Takata-Tomokuni, Akiko; Katsuyama, Hironobu; Otsuki, Takemi

doi:10.1016/j.imlet.2004.11.005

Cited by 35 publications

(32 citation statements)

References 31 publications

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“…2-A) and the message level (Wu, 2005). Although the data is not shown here, it was evident that PHA can stimulate T cells and that CD69 expression was observed at day 1 as the peak and then gradually reduced until day 5 (Wu, 2005). Additionally, chrysotile A was not able to induce CD69 expression (Wu, 2005).…”

Section: Chronic Activation Of Tresp By Exposure To Silicamentioning

confidence: 60%

“…Results showed that only silica can upregulate CD69 expression in T cells slowly and gradually in a dose-dependent manner in regard to cell surface expression (as shown in Fig. 2-A) and the message level (Wu, 2005). Although the data is not shown here, it was evident that PHA can stimulate T cells and that CD69 expression was observed at day 1 as the peak and then gradually reduced until day 5 (Wu, 2005).…”

Section: Chronic Activation Of Tresp By Exposure To Silicamentioning

confidence: 77%

“…To investigate the hypothesis that silica chronically activates Tresp, we first examined the in vitro activation of Tresp by exposure to silica (Wu, 2005). Freshly isolated PBMCs from HVs were cultured with or without phytohaemagglutinin (PHA), Min-U-silica (25 or 50 µg/ml) or chrysotile A (an asbestos, 50 µg/ml) for ten days.…”

Section: Chronic Activation Of Tresp By Exposure To Silicamentioning

confidence: 99%

See 2 more Smart Citations

Immunological Effects of Silica and Related Dysregulation of Autoimmunity

Kumagai¹,

Hayashi²,

Maeda³

et al. 2011

Autoimmune Disorders - Pathogenetic Aspects

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Section: Chronic Activation Of Tresp By Exposure To Silicamentioning

confidence: 60%

Section: Chronic Activation Of Tresp By Exposure To Silicamentioning

confidence: 77%

Section: Chronic Activation Of Tresp By Exposure To Silicamentioning

confidence: 99%

See 1 more Smart Citation

Immunological Effects of Silica and Related Dysregulation of Autoimmunity

Kumagai¹,

Hayashi²,

Maeda³

et al. 2011

Autoimmune Disorders - Pathogenetic Aspects

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“…This attenuation may be caused by the substitution of the CD4+25+ fraction by chronically activated T cells due to their chronic and recurrent exposure to silica, as shown by our in vitro finding of the slower activation of T cells by silica (41).…”

Section: Alterations Of Fas-related Molecules and Cd4+25+ Regulatory mentioning

confidence: 69%

“…VII) In vitro exposure of T cells derived from HD to silica causes a slow but precise activation of these cells, as indicated by the expression of CD69, a typical early marker of T cell activation (41).…”

Section: Alterations Of Fas-related Molecules and Cd4+25+ Regulatory mentioning

confidence: 99%

Keynote lecture in the 13th Japanese Society of Immunotoxicology (JSIT 2006)

Otsuki

Miura

Maeda

et al. 2007

Environ Health Prev Med

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Silica and silicates may disturb immune functions such as autoimmunity and tumor immunity, because people who are exposed to the materials sometimes develop autoimmune and malignant diseases, respectively. Although silica-induced disorders of autoimmunity have been explained as adjuvant-type effects of silica, more precise analyses are needed and should reflect the recent progress in immunomolecular findings. A brief summary of our investigations related to the immunological effects of silica/asbestos is presented. Recent advances in immunomolecular studies led to detailed analyses of the immunological effects of asbestos and silica. Both affect immuno-competent cells and these effects may be associated with the pathophysiological development of complications in silicosis and asbestos-exposed patients such as the occurrence of autoimmune disorders and malignant tumors, respectively. In addition, immunological analyses may lead to the development of new clinical tools for the modification of the pathophysiological aspects of diseases such as the regulation of autoimmunity or tumor immunity using cell-mediated therapies, various cytokines, and molecule-targeting therapies. In particular, as the incidence of asbestos-related malignancies is increasing and such malignancies have been a medical and social problem since the summer in 2005 in Japan, efforts should be focused on developing a cure for these diseases to eliminate the nation wide anxiety about these malignancies.

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Medical‐grade silicone induces release of proinflammatory cytokines in peripheral blood mononuclear cells without activating T cells

Miró-Mur¹,

Hindié²,

Kandhaya‐Pillai³

et al. 2009

J Biomed Mater Res

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For more than 40 years, silicone implants had been employed in aesthetic, cosmetic medicine, and plastic surgery. Although adverse reactions produced by these products are rare, cases of immuno-mediated reactions have been reported. To evaluate the aspects of immuno-reactivity to medical-grade silicone dermal filler, peripheral blood mononuclear cells (PBMC) of 39 individuals were studied. PBMC used include individuals with silicone injection-related delayed adverse reactions, with silicone injections, and healthy control. Silicone induced production of TNF-alpha and IL-6 in all three groups. Notably, elevated production of IL-6 was observed in nonstimulated PBMC and also the percentage of CD4(+)CD69(+) T cells was higher in PHA-stimulated PBMC from individuals with silicone injection-related adverse reactions when compared with other two groups. However, IFN-gamma was not released in silicone-stimulated or silicone+LPS-stimulated PBMC from any group and no production of IL-2 was measured indicating no proliferative response of PBMC. Subsequently, no CD4(+)CD69(+) T cells were observed in these conditions. Finally, the inflammatory response in silicone-stimulated cultures of monocyte-derived macrophages with autologous lymphocytes is lesser than that observed in PBMC. In conclusion, silicone induces a release of proinflammatory cytokines but does not act as a polyclonal activator of CD4(+) T cells. Thus, silicone is mounting an immune response in individuals with silicone-related adverse effects but is not silicone antigen-dependent.

show abstract

Induction of CD69 antigen expression in peripheral blood mononuclear cells on exposure to silica, but not by asbestos/chrysotile-A

Cited by 35 publications

References 31 publications

Immunological Effects of Silica and Related Dysregulation of Autoimmunity

Immunological Effects of Silica and Related Dysregulation of Autoimmunity

Keynote lecture in the 13th Japanese Society of Immunotoxicology (JSIT 2006)

Medical‐grade silicone induces release of proinflammatory cytokines in peripheral blood mononuclear cells without activating T cells

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