| First Author | Bachmann MF | Year | 2007 |
| Journal | Eur J Immunol | Volume | 37 |
| Issue | 6 | Pages | 1502-12 |
| PubMed ID | 17492805 | Mgi Jnum | J:123518 |
| Mgi Id | MGI:3718762 | Doi | 10.1002/eji.200637023 |
| Citation | Bachmann MF, et al. (2007) Differential role of IL-2R signaling for CD8+ T cell responses in acute and chronic viral infections. Eur J Immunol 37(6):1502-12 |
| abstractText | IL-2 is a cytokine with multiple and even divergent functions; it has been described as a key cytokine for in vitro T cell proliferation but is also essential for down-regulating T cell responses by inducing activation-induced cell death as well as regulatory T cells. The in vivo analysis of IL-2 function in regulating specific T cell responses has been hampered by the fact that mice deficient in IL-2 or its receptors develop lymphoproliferative diseases and/or autoimmunity. Here we generated chimeric mice harboring both IL-2R-competent and IL-2R-deficient T cells and assessed CD8+ T cell induction, function and maintenance after acute or persistent viral infections. Induction and maintenance of CD8+ T cells were relatively independent of IL-2R signaling during acute/resolved viral infection. In marked contrast, IL-2 was crucial for secondary expansion of memory CD8+ T cells and for the maintenance of virus-specific CD8+ T cells during persistent viral infections. Thus, depending on the chronicity of antigen exposure, IL-2R signaling is either essential or largely dispensable for induction and maintenance of virus-specific CD8+ T cell responses. |
