Kazuhito Toyooka. Ph.D.


Assistant professor


Curriculum vitae



215-991-8288


Department of Neurobiology and Anatomy


Drexel University College of Medicine


2900 W. Queen Lane, Room186



Differential involvement of a Fas-CPP32-like protease pathway in apoptosis of TCR/CD9-costimulated, naive T cells and TCR-restimulated, activated T cells.


Journal article


C. S. Park, Y. Yashiro, X. Tai, K. Toyo-oka, T. Hamaoka, H. Yagita, K. Okumura, S. Neben, H. Fujiwara
Journal of immunology, 1998

Semantic Scholar DOI PubMed
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APA
Park, C. S., Yashiro, Y., Tai, X., Toyo-oka, K., Hamaoka, T., Yagita, H., … Fujiwara, H. (1998). Differential involvement of a Fas-CPP32-like protease pathway in apoptosis of TCR/CD9-costimulated, naive T cells and TCR-restimulated, activated T cells. Journal of Immunology.

Chicago/Turabian
Park, C. S., Y. Yashiro, X. Tai, K. Toyo-oka, T. Hamaoka, H. Yagita, K. Okumura, S. Neben, and H. Fujiwara. “Differential Involvement of a Fas-CPP32-like Protease Pathway in Apoptosis of TCR/CD9-Costimulated, Naive T Cells and TCR-Restimulated, Activated T Cells.” Journal of immunology (1998).

MLA
Park, C. S., et al. “Differential Involvement of a Fas-CPP32-like Protease Pathway in Apoptosis of TCR/CD9-Costimulated, Naive T Cells and TCR-Restimulated, Activated T Cells.” Journal of Immunology, 1998.


Abstract

Our previous study showed that CD9 costimulation of TCR-triggered naive T cells elicits activation ([3H]TdR incorporation) that is similar to CD28 costimulation; however, unlike CD28 costimulation, CD9 costimulation results in apoptosis of these previously activated T cells. Here, we investigated whether the apoptosis occurring after TCR/CD9 stimulation is associated with a death pathway involving Fas stimulation and Fas-mediated caspase activation as observed in activation-induced cell death (AICD). In contrast to AICD, the apoptosis resulting from TCR/CD9 stimulation in C57BL/6 T cells was independent of Fas, because this form of apoptosis was not prevented by anti-Fas ligand mAb and was also induced in MRL/lpr T cells. AICD was observed at 12 h after the restimulation of activated T cells with anti-CD3 and reached a peak level at 24 h after this restimulation. CPP32-like protease activity was detected during AICD. Although TCR/CD9 stimulation-associated apoptosis was observed at 24 h after the stimulation of naive T cells and reached a peak level at 36 h after this stimulation, CPP32-like protease activity in these T cells was only marginal at all time points. Nevertheless, both forms of apoptosis were prevented similarly by two different peptide-based caspase inhibitors. These results indicate that the apoptosis that follows the T cell activation which is induced as a result of CD9 costimulation does not involve a Fas-CPP32-like protease pathway, but suggest that different caspase members are likely to be critical in this form of apoptosis.


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