Involvement of IL-10 and Bcl-2 in resistance against an asbestos-induced apoptosis of T cells

Apoptosis. 2006 Oct;11(10):1825-35. doi: 10.1007/s10495-006-9235-4.


To analyze the possibility that immunological alteration in asbestos-related diseases (ARDs) such as asbestosis (ASB) and malignant mesothelioma (MM) may affect the progression of cancers, a human adult T cell leukemia virus-immortalized T cell line (MT-2Org) was continuously exposed to 10 mug/ml of chrysotile-B (CB), an asbestos. After at least 8 months of exposure, the rate of apoptosis in the cells became very low and the resultant subline was designated MT-2Rst. The MT-2Rst cells were characterized by (i) enhanced expression of bcl-2, with regain of apoptosis-sensitivity by reduction of bcl-2 by siRNA, (ii) excess IL-10 secretion and expression, and (iii) activation of STAT3 that was inhibited by PP2, a specific inhibitor of Src family kinases. These results suggested that the contact between cells and asbestos may affect the human immune system and trigger a cascade of biological events such as activation of Src family kinases, enhancement of IL-10 expression, STAT3 activation and Bcl-2 overexpression. This speculation was partially confirmed by the detection of elevated bcl-2 expression levels in CD4 + peripheral blood T cells from patients with MM compared with those from patients with ASB or healthy donors. Further studies will be required to verify the role of T cells with enhanced bcl-2 expression in tumor progression induced by asbestos exposure.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Apoptosis Regulatory Proteins / metabolism
  • Asbestos / adverse effects*
  • Asbestos, Serpentine / adverse effects
  • Asbestos, Serpentine / pharmacology
  • Asbestosis / blood
  • Cell Proliferation
  • Cells, Cultured
  • Cytokines / biosynthesis
  • Humans
  • Interleukin-10 / metabolism
  • Interleukin-10 / physiology*
  • Leukocytes / pathology
  • Mesothelioma / blood
  • Models, Biological
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / physiology*
  • STAT3 Transcription Factor / metabolism
  • T-Lymphocytes / drug effects*
  • T-Lymphocytes / metabolism
  • bcl-2-Associated X Protein / metabolism
  • src-Family Kinases / metabolism


  • Apoptosis Regulatory Proteins
  • Asbestos, Serpentine
  • Cytokines
  • Proto-Oncogene Proteins c-bcl-2
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • bcl-2-Associated X Protein
  • Interleukin-10
  • Asbestos
  • src-Family Kinases