| First Author | Hotchkiss RS | Year | 2000 |
| Journal | J Immunol | Volume | 164 |
| Issue | 7 | Pages | 3675-80 |
| PubMed ID | 10725725 | Mgi Jnum | J:123711 |
| Mgi Id | MGI:3719319 | Doi | 10.4049/jimmunol.164.7.3675 |
| Citation | Hotchkiss RS, et al. (2000) p53-dependent and -independent pathways of apoptotic cell death in sepsis. J Immunol 164(7):3675-80 |
| abstractText | Sepsis induces extensive apoptosis of lymphocytes, which may be responsible for the profound immune suppression of the disorder. Two potential pathways of sepsis-induced lymphocyte apoptosis, Fas and p53, were investigated. Lymphocyte apoptosis was evaluated 20-22 h after sepsis by annexin V or DNA nick-end labeling. Fas receptor-deficient mice had no protection against sepsis-induced apoptosis in thymocytes or splenocytes. p53 knockout mice (p53-/-) had complete protection against thymocyte apoptosis but, surprisingly, had no protection in splenocytes. p53-/- mice had no improvement in sepsis survival compared with appropriately matched control mice with sepsis. We conclude that both p53-dependent and p53-independent pathways of cell death exist in sepsis. This differential apoptotic response of thymocytes vs splenocytes in p53-/- mice suggests that either the cellular response or the death-inducing signal is cell-type specific in sepsis. The fact that p53-/- lymphocytes of an identical subtype (CD8-CD4+) were protected in thymi but not in spleens indicates that cell susceptibility to apoptosis differs depending upon other unidentified factors. |
