| First Author | Xiao Z | Year | 2009 |
| Journal | J Immunol | Volume | 182 |
| Issue | 5 | Pages | 2786-94 |
| PubMed ID | 19234173 | Mgi Jnum | J:146256 |
| Mgi Id | MGI:3837094 | Doi | 10.4049/jimmunol.0803484 |
| Citation | Xiao Z, et al. (2009) Programming for CD8 T cell memory development requires IL-12 or type I IFN. J Immunol 182(5):2786-94 |
| abstractText | Inflammation can have both positive and negative effects on development of CD8 T cell memory, but the relative contributions and cellular targets of the cytokines involved are unclear. Using CD8 T cells lacking receptors for IL-12, type I IFN, or both, we show that these cytokines act directly on CD8 T cells to support memory formation in response to vaccinia virus and Listeria monocytogenes infections. Development of memory to vaccinia is supported predominantly by IL-12, whereas both IL-12 and type I IFN contribute to memory formation in response to Listeria. In contrast to memory formation, the inability to respond to IL-12 or type I IFN had a relatively small impact on the level of primary expansion, with at most a 3-fold reduction in the case of responses to Listeria. We further show that programming for memory development by IL-12 is complete within 3 days of the initial naive CD8 T cell response to Ag. This programming does not result in formation of a population that expresses killer cell lectin-like receptor G1, and the majority of the resulting memory cells have a CD62L(high) phenotype characteristic of central memory cells. Consistent with this, the cells undergo strong expansion upon rechallenge and provide protective immunity. These data demonstrate that IL-12 and type I IFN play an essential early role in determining whether Ag encounter by naive CD8 T cells results in formation of a protective memory population. |
