| First Author | Maxwell JR | Year | 2006 |
| Journal | J Immunol | Volume | 177 |
| Issue | 1 | Pages | 234-45 |
| PubMed ID | 16785519 | Mgi Jnum | J:134442 |
| Mgi Id | MGI:3785693 | Doi | 10.4049/jimmunol.177.1.234 |
| Citation | Maxwell JR, et al. (2006) IL-18 bridges innate and adaptive immunity through IFN-gamma and the CD134 pathway. J Immunol 177(1):234-45 |
| abstractText | IL-18 induces inflammation resulting in either enhanced protection from pathogens or exacerbation of autoimmunity, and T cells are profoundly activated during these responses. How IL-18 influences T cell activation is unknown, but this study in mice shows that IL-18 boosted Ag-specific T cell clonal expansion of effector T cells and induced a subpopulation of IFN-gamma superproducing T cells. Commitment to IFN-gamma production through IL-18 was independent of NK cells and IL-12 but dependent on host-derived IFN-gamma. To determine how expansion of these effectors occurred, IL-18 was shown to induce OX40L on dendritic cells, whereas peptide stimulation induced CD134 (OX40) on specific T cells. CD134 blockade inhibited T cell effector expansion thereby reducing the number of IFN-gamma superproducers by 12-fold. Thus, independent of IL-12, IL-18 impacts T cell immunity throughout lymphoid and nonlymphoid tissue by bridging the innate and adaptive arms of the immune system through IFN-gamma and the CD134 costimulatory pathway. |
