| First Author | Intlekofer AM | Year | 2008 |
| Journal | Science | Volume | 321 |
| Issue | 5887 | Pages | 408-11 |
| PubMed ID | 18635804 | Mgi Jnum | J:137655 |
| Mgi Id | MGI:3801396 | Doi | 10.1126/science.1159806 |
| Citation | Intlekofer AM, et al. (2008) Anomalous type 17 response to viral infection by CD8+ T cells lacking T-bet and eomesodermin. Science 321(5887):408-11 |
| abstractText | When intracellular pathogens invade mammalian hosts, naive CD8+ T cells differentiate into cytotoxic killers, which lyse infected target cells and secrete cytokines that activate intracellular microbicides. We show that CD8+ T cells deficient in the transcription factors T-bet and eomesodermin (Eomes) fail to differentiate into functional killers required for defense against lymphocytic choriomeningitis virus. Instead, virus-specific CD8+ T cells lacking both T-bet and Eomes differentiate into an interleukin-17-secreting lineage, reminiscent of the helper T cell fate that has been implicated in autoimmunity and extracellular microbial defense. Upon viral infection, mice with T cells lacking both T-bet and Eomes develop a CD8+ T cell-dependent, progressive inflammatory and wasting syndrome characterized by multi-organ infiltration of neutrophils. T-bet and Eomes, thus, ensure that CD8+ T cells adopt an appropriate course of intracellular rather than extracellular destruction. |
