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Articles by O. Kanagawa
Total Records ( 2 ) for O. Kanagawa
  M Tomura , Y. S Mori , R Watanabe , M Tanaka , A Miyawaki and O. Kanagawa
 

Fluorescent protein that detects caspase-3 activation was used for the time-lapse observation of CTL–target cell interaction. In the target cells transfected with SCAT3.1 (caspase-3-sensitive fusion protein) complementary DNA, caspase-3 activation can be detected significantly earlier than the commonly used annexin-V binding that detects membrane change in apoptotic cells. Moreover, during the cytolytic interaction between OE4 CTL and W3 tumor target cells, detachment of CTL from the target cells occurred prior to caspase-3 activation and death of the target cells, indicating very early sensing of apoptotic target cells by CTL. This early detachment of OE4 CTL from W3 target cells was inhibited by the expression of CD80 co-stimulatory molecule on the target cells. Taken together, time-lapse observation of cellular interaction with functional probe, SCAT3.1 provides new kinetic information and demonstrates that co-stimulatory molecules regulate the kinetics of CTL–target cell interaction.

  Y Mori , T Kodaka , T Kato , E. M Kanagawa and O. Kanagawa
 

IFN- signaling-deficient non-obese diabetic (NOD) mice develop diabetes with similar kinetics to those of wild-type NOD mice. However, the immunization of IFN- signaling-deficient NOD mice with CFA failed to induce long-term protection, whereas wild-type NOD mice receiving CFA remained diabetes-free. CFA also failed to protect IFN- receptor-deficient (IFN-R–/–) NOD mice from the autoimmune rejection of transplanted islets, as it does in diabetic NOD mice, and from disease transfer by spleen cells from diabetic NOD mice. These data clearly show that the pro-inflammatory cytokine IFN- is necessary for the CFA-mediated protection of NOD mice from diabetes. There is no difference in the Th1/Th17 balance between IFN-R–/– NOD and wild-type NOD mice. There is also no difference in the total numbers and percentages of regulatory T (Treg) cells in the lymph node CD4+ T-cell populations between IFN-R–/– NOD and wild-type NOD mice. However, pathogenic T cells lacking IFN-R are resistant to the suppressive effect of Treg cells, both in vivo and in vitro. Therefore, it is likely that CFA-mediated protection against diabetes development depends on a change in the balance between Treg cells and pathogenic T cells, and IFN- signaling seems to control the susceptibility of pathogenic T cells to the inhibitory activity of Treg cells.

 
 
 
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