| First Author | Setoguchi R | Year | 2009 |
| Journal | J Immunol | Volume | 183 |
| Issue | 7 | Pages | 4467-74 |
| PubMed ID | 19734230 | Mgi Jnum | J:152786 |
| Mgi Id | MGI:4359976 | Doi | 10.4049/jimmunol.0901428 |
| Citation | Setoguchi R, et al. (2009) ThPOK derepression is required for robust CD8 T cell responses to viral infection. J Immunol 183(7):4467-74 |
| abstractText | In the thymus, the transcription factor ThPOK is essential for the development of the CD4 helper T cell lineage, whereas active repression of ThPOK is critical for the development of the CD8 cytotoxic T cell lineage. ThPOK gene silencing is thought to be irreversible in peripheral CD8 T cells. We noticed that ThPOK repression is readily abrogated upon in vitro TCR stimulation of peripheral CD8 T cells. This observation prompted us to investigate a role for ThPOK in the CD8 T cell response to an acute viral infection. We observed that a functional deficiency of ThPOK does not affect CD8 T cell differentiation into effector T cells and the long-term persistence of Ag-specific memory T cells. However, in the absence of functional ThPOK, clonal expansion is significantly less in both primary and secondary CD8 T cell responses. Long-lived, Ag-specific CD8 T cells with a functional deficiency in ThPOK fail to produce high amounts of IL-2 and also fail to express high levels of granzyme B upon rechallenge. Our data reveal an unexpected role for ThPOK in CD8 T cells in promoting expansion and boosting the response to antigenic challenge. |
