期刊
JOURNAL OF IMMUNOLOGY
卷 177, 期 1, 页码 234-245出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.1.234
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- NCI NIH HHS [R01 CA 102577] Funding Source: Medline
- NIAID NIH HHS [R01 AI 42858, R01 AI042858, R01 AI 52108, R01 AI042858-06, R01 AI042858-05, P01 AI 56172] Funding Source: Medline
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.
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