Asbestos-related cancers such as malignant mesothelioma and lung cancer are an important issue in Japan and the world. There are many conflicts concerning economical considerations and medical evidence for these cancers, and much confusion regarding details of the pathological mechanisms of asbestos-induced cancers. For example, there is uncertainty concerning the degree of danger of the iron-absent chrysotile (white) asbestos compared with iron-containing crocidolite (blue) and amosite (brown) asbestos. However, regarding bad prognosis of mesothelioma, medical approaches to ensure recognition of the biological effects of asbestos and the pathological mechanisms of asbestos-induced carcinogenesis, as well as clinical trials to detect the early stage of mesothelioma, should result in better preventions and the cure of asbestos-related malignancies. It is on the basis of these considerations that our group has been investigating the immunological effects of asbestos in relation to reduction of tumor immunity.
Methods
A human HTLV-1 immortalized polyclonal T cell line, MT-2 has been exposed continuously and low-dose of chrysotile, an asbestos, for the establishment of cell line model of asbestos exposure. The important chemokine receptor in tumor immunity with relationship to IFN-gamma, CXCR3 expression in cell lines as well as in vitro exposure of T cell from healthy donor, and asbestos-exposed plaque or mesothelioma patients.
Results
Continuously exposed subline of MT-2 and in vitro exposed T cell from healthy donor revealed reduction of IFN-gamma production and CXCR3 expression. In addition, peripheral T cell also showed decreased expression of CXCR3 in plaque and mesothelioma patinets.
Discussion
Asbestos can reduce CXCR3 expression and IFN-gamma production and may cause reduction of tumor immunity involved in asbestos-induced carcinogenesis and cancer progression.