| First Author | Lodolce JP | Year | 2001 |
| Journal | J Exp Med | Volume | 194 |
| Issue | 8 | Pages | 1187-94 |
| PubMed ID | 11602647 | Mgi Jnum | J:72171 |
| Mgi Id | MGI:2151959 | Doi | 10.1084/jem.194.8.1187 |
| Citation | Lodolce JP, et al. (2001) T cell-independent interleukin 15ralpha signals are required for bystander proliferation. J Exp Med 194(8):1187-94 |
| abstractText | Cytokine driven or 'bystander' proliferation of T cells occurs in vivo independently of major histocompatibility complex-T cell receptor interactions. This process may be important for supporting T cell homeostasis and facilitating T cell responses to microbial antigens, and may involve the cytokine interleukin (IL)-15. In this study, we find that IL-15Ralpha-deficient (IL-15Ralpha(-/)-) mice fail to undergo poly I:C or IL-15 driven bystander proliferation of CD8(+) T cells. Surprisingly, IL-15Ralpha(-/)- CD8(+) T cells proliferate in response to poly I:C when adoptively transferred into normal mice, and normal CD8(+) T cells fail to proliferate in IL-15Ralpha(-/)- mice. Normal mice reconstituted with IL-15Ralpha(-/)- bone marrow cells also fail to exhibit bystander responses. Thus, CD8(+) T cell independent IL-15Ralpha signals from radiation sensitive hematopoietic cells are likely required for bystander responses. Moreover, normal CD8(+) T cells proliferate in IL-15Ralpha(-/)- mice after treatment with IL-15. Therefore, IL-15Ralpha signals may mediate a positive feedback loop involving the further physiological production of IL-15. These findings provide new insights into how IL-15Ralpha supports memory phenotype CD8(+) T cell proliferation, and suggest novel mechanisms by which memory CD8(+) T cells are maintained in vivo. |
