| First Author | Spaner D | Year | 1998 |
| Journal | J Immunol | Volume | 160 |
| Issue | 6 | Pages | 2655-64 |
| PubMed ID | 9510164 | Mgi Jnum | J:123740 |
| Mgi Id | MGI:3719348 | Doi | 10.4049/jimmunol.160.6.2655 |
| Citation | Spaner D, et al. (1998) A role for perforin in activation-induced cell death. J Immunol 160(6):2655-64 |
| abstractText | The granule exocytosis pathway of T cell cytotoxicity is absent in mice whose perforin gene has been ablated by targeted mutagenesis. The ability of activated naive T cells to undergo apoptosis in vitro following reaggregation of the TCR complex with anti-TCR mAbs via a Fas-independent pathway was found to be defective in the absence of perforin. Protection from death was most marked in CD8+ T cells. In wild-type cells, perforin was expressed at the same time that apoptosis occurred, and blockade of perforin expression by either incubation with perforin antisense oligonucleotides or with anti-IL-2 Abs resulted in increased viability of activated T cells. The role of perforin was not via perforin-dependent fratricidal killing. The results suggest a model in which perforin acts internally to cause a form of activation-induced T cell death distinct from that caused by members of the TNFR superfamily. |
