| First Author | Koenig A | Year | 2012 |
| Journal | Immunology | Volume | 135 |
| Issue | 4 | Pages | 276-86 |
| PubMed ID | 22117649 | Mgi Jnum | J:184101 |
| Mgi Id | MGI:5320255 | Doi | 10.1111/j.1365-2567.2011.03540.x |
| Citation | Koenig A, et al. (2012) Proliferating gammadelta T cells manifest high and spatially confined caspase-3 activity. Immunology 135(4):276-86 |
| abstractText | Caspase-8 serves two paradoxical roles in T lymphocytes: it initiates apoptosis following death receptor engagement, and is also indispensible for proliferation following T-cell antigen receptor (TCR) signalling. These opposing processes appear to be controlled by both spatial and quantitative differences in caspase-8 activation. Given differences in the turnover of T-cell subsets, we compared caspase activity and susceptibility to cell death following TCR restimulation in murine CD4(+) and CD8(+) alphabeta T cells and gammadelta T cells. We observed a spectrum of caspase activity in non-dying effector T cells in which CD4(+) T cells manifested the lowest levels of active caspases whereas gammadelta T cells manifested the highest levels. Further analysis revealed that most of the difference in T-cell subsets was the result of high levels of active caspase-3 in non-dying effector gammadelta T cells. Despite this, gammadelta T cells manifested little spontaneous or CD3 restimulation-induced cell death as the result of confinement of active caspases to the cell membrane. By contrast, CD4(+) T cells were highly sensitive to CD3-induced cell death, associated with the appearance of active caspases in the cytoplasm and cleavage of the caspase substrates Bid and ICAD. Hence, the location and amount of active caspases distinguishes effector T-cell subsets and profoundly influences the fate of the T-cell response. |
