Activation of human CD4+CD45RA+ T cells by chrysotile asbestos in vitro

Kinugawa, Keigo; Ueki, Ayako; Yamaguchi, M; Watanabe, Yoshiki; Kawakami, Yasuhiko; Hyodoh, Fuminori; Tsushima, Hirofumi

doi:10.1016/0304-3835(92)90221-g

Cited by 11 publications

(13 citation statements)

References 18 publications

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“…Rustin et al [23] attempted to demonstrate the differences between PSS in the patients with silicosis and idiopathic progressive sclerosis, and no clinical, immunological or serological differences were detected between the two types of sclerosis. In previous papers [9,24], we reported a finding of polyclonal human T cell activation by silicate as a superantigen in virro. Superantigens, e.g.…”

Section: Discussionmentioning

confidence: 99%

Elevated soluble Fas/APO-1 (CD95) levels in silicosis patients without clinical symptoms of autoimmune diseases or malignant tumours

Tomokuni

Aikoh

Matsuki

et al. 1997

Clinical and Experimental Immunology

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SUMMARYSoluble Fas (sFas) is produced as translation products of alternative mRNA splicing, and antagonizes the membranous Fas molecule in Faspas ligand interactions. We investigated the serum sFas levels in 64 Japanese silicosis patients with no clinical symptoms of autoimmune diseases or malignant tumours, using ELISA for sFas. The serum sFas levels in the silicosis patients were significantly higher than those in healthy volunteers. Elevated serum sFas levels were also detected in patients with systemic lupus erythematosus but, unexpectedly, no difference was observed in sFas levels between progressive systemic sclerosis patients and healthy volunteers. On the other hand, there was no significant difference in the expression of Fas on peripheral blood lymphocytes between the patients with silicosis and agematched healthy volunteers. These observations provided the first evidence that serum sFas levels are elevated in silicosis patients without clinical symptoms of autoimmune diseases or malignant tumours. It remains to be clarified whether patients with elevated sFas levels have a tendency to develop autoimmune diseases later, or whether some other distinct factor(s) is necessary to initiate the progression of autoimmune diseases.

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Section: Discussionmentioning

confidence: 99%

Elevated soluble Fas/APO-1 (CD95) levels in silicosis patients without clinical symptoms of autoimmune diseases or malignant tumours

Tomokuni

Aikoh

Matsuki

et al. 1997

Clinical and Experimental Immunology

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“…Howe ver, it is worth-considering that the occurrence of incurable and rapidly progressing malignancies, even though there are very long latent stages of approximately 30 to 40 years, may be accelerated by a decline in tumor immunity. We also studied the immunological effects of asbestos using chrysotile fibers (5)(6)(7)(8) and activation of mitochondrial pathway similar to the killing process of pulmonary alveolar and mesothelial cells by asbestos (8). Therefore, since it was necessary to observe the immunological effects of long-term and low-dose exposure to asbestos, the MT-20rg line was employed.…”

Section: Tcr-vj3 Analyses Of Silica and Asbestos-related Disordersmentioning

confidence: 99%

“…In addition, PBMCs from healthy donors exposed to asbestos in culture underwent apoptosis (5)(6)(7)(8). However, many patients with asbestosis have had chronic, occupational and recurrent exposure to silicates.…”

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confidence: 99%

Expression of the T Cell Receptor Vβ Repertoire in a Human T Cell Resistant to Asbestos-Induced Apoptosis and Peripheral Blood T Cells from Patients with Silica and Asbestos-Related Diseases

Nishimura

Miura

Maeda

et al. 2006

Int J Immunopathol Pharmacol

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To explore the effects of asbestos and silica on the human immune system, an experimental model of lowdose and long-term exposure was established using a human UTLV-l-immortalized polyclonal T cell line, MT-2 (MT-20rg). MT-2 cells were continuously exposed to asbestos at a concentration (10 ug/ml) which does not induce complete cell death during short-term exposure. After acquiring resistance to CD-induced apoptosis (designated MT-2Rst), an immunological comparison was made between the MT-20rg and MT2Rst lines in terms of T cell receptor-VO (TcR-VO) expression. MT-2Rst cells showed excess expression of various TcR-VO, although TcR-VO-overpresenting cells were characterized as undergoing apoptosis due to first contact with CD. Patients with asbestos-related diseases (AJ{D), such as asbestosis and malignant mesothelioma, were compared with silicosis (SIL) patients as a disease control and with healthy donors (UD). SIL and ARD not only differed in their causative materials, silica and asbestos as mineral silicates, but also in terms of complications; autoimmune disorders in SIL and tumors in ARD. ARD patients showed a restricted overpresentation ofTcR-VO without clonal expansion, whereas SIL patients revealed significant overpresentation of TcR-VO 7.2. These experimental and clinical analyses indicate the superantigenic and dysregulation of autoimmunity-inducing effects of asbestos and silica, respectively.Asbestos (e.g. chrysotile, crocidolite and amosite) is known to cause malignant lung cancer or mesothelioma. The International Agency for Research on Cancer (IARC) categorizes both asbestos and crystalline silica as group I carcinogens (1). According to the IARC classification, asbestos affects alveolar epithelial and mesothelial cells. There have been many studies concerning asbestosinduced apoptosis in these cells. Experimentally, these cells have undergone apoptosis on a relatively high-level, short-term exposure to asbestos via the production of ROS and RNS with activation of the mitochondrial apoptotic pathway (2-4). Thus, it has been considered that during low-level and long-term exposure to asbestos in the human body, alveolar epithelial and mesothelial cells escape from

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“…Stomach cancer is the most consistently reported outcome of GIT-related pathologies due to asbestos exposure (Kjaerheim et al, 2005; Kanarek et al, 1980; Polissar et al, 1983; Andersen et al, 1993; Hillerdal, 1980). However, there are reports of increased colon (Kjaerheim et al, 2005; Germani et al, 1999) and esophageal cancer (Kang et al, 1997) in response to asbestos.…”

Section: Gastrointestinal Effects Of Asbestosmentioning

confidence: 99%

“…However, there are reports of increased colon (Kjaerheim et al, 2005; Germani et al, 1999) and esophageal cancer (Kang et al, 1997) in response to asbestos. In contrast, additional studies evaluating environmental exposure to asbestos via the drinking water noted no increased disease of the GIT on the whole, including stomach cancer (Harrington et al, 1978; Levy et al, 1976; Browne et al, 2005; Hodgson & Jones, 1986; Toft & Meek, 1983).…”

Section: Gastrointestinal Effects Of Asbestosmentioning

confidence: 99%

Nonpulmonary Outcomes of Asbestos Exposure

Bunderson-Schelvan

Pfau

Crouch

et al. 2011

Journal of Toxicology and Environmental Health, Part B

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The adverse pulmonary effects of asbestos are well accepted in scientific circles. However, the extrapulmonary consequences of asbestos exposure are not as clearly defined. In this review the potential for asbestos to produce diseases of the peritoneum, immune, gastrointestinal (GIT), and reproductive systems are explored as evidenced in published, peer-reviewed literature. Several hundred epidemiological, in vivo, and in vitro publications analyzing the extrapulmonary effects of asbestos were used as sources to arrive at the conclusions and to establish areas needing further study. In order to be considered, each study had to monitor extrapulmonary outcomes following exposure to asbestos. The literature supports a strong association between asbestos exposure and peritoneal neoplasms. Correlations between asbestos exposure and immune-related disease are less conclusive; nevertheless, it was concluded from the combined autoimmune studies that there is a possibility for a higher-than-expected risk of systemic autoimmune disease among asbestos-exposed populations. In general, the GIT effects of asbestos exposure appear to be minimal, with the most likely outcome being development of stomach cancer. However, IARC recently concluded the evidence to support asbestos-induced stomach cancer to be “limited.” The strongest evidence for reproductive disease due to asbestos is in regard to ovarian cancer. Unfortunately, effects on fertility and the developing fetus are under-studied. The possibility of other asbestos-induced health effects does exist. These include brain-related tumors, blood disorders due to the mutagenic and hemolytic properties of asbestos, and peritoneal fibrosis. It is clear from the literature that the adverse properties of asbestos are not confined to the pulmonary system.

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Activation of human CD4+CD45RA+ T cells by chrysotile asbestos in vitro

Cited by 11 publications

References 18 publications

Elevated soluble Fas/APO-1 (CD95) levels in silicosis patients without clinical symptoms of autoimmune diseases or malignant tumours

Elevated soluble Fas/APO-1 (CD95) levels in silicosis patients without clinical symptoms of autoimmune diseases or malignant tumours

Expression of the T Cell Receptor Vβ Repertoire in a Human T Cell Resistant to Asbestos-Induced Apoptosis and Peripheral Blood T Cells from Patients with Silica and Asbestos-Related Diseases

Nonpulmonary Outcomes of Asbestos Exposure

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