Differential capacities of CD4(+), CD8(+), and CD4(-)CD8(-) T cell subsets to express IL-18 receptor and produce IFN-gamma in response to IL-18

作者:Tomura M; Maruo S; Mu J; Zhou XY; Ahn HJ; Hamaoka T; Okamura H; Nakanishi K; Clark S; Kurimoto M; Fujiwara H*
来源:The Journal of Immunology, 1998, 160(8): 3759-3765.
DOI:10.4049/jimmunol.160.8.3759

摘要

IL-12 and IL-18 have the capacity to stimulate IFN-gamma production by T cells, Using a T cell clone, we reported that IL-18 responsiveness is generated only after exposure to IL-12, Here, we investigated the induction of IL-18 responsiveness in resting CD8(+), CD4(+), and CD4(-)CD8(-) T cells, Resting T cells respond to neither IL-12 nor IL-18, After stimulation with anti-CD3 plus anti-CD28 mAbs, CD8(+), CD4(+), and CD4(-)CD8(-) T cells expressed IL-12R, but not IL-18R, and produced IFN-gamma in response to IL-12, Cultures of T cells with anti-CD3/anti-CD28 in the presence of rIL-12 induced IL-18R expression and IL-18-stimulated IFN-gamma production, which reached higher levels than that induced by IL-12 stimulation, However, there was a substantial difference in the expression of IL-18R and IL-18-stimulated IFN-gamma production among T cell subsets, CD4(+) cells expressed marginal levels of IL-18R and produced small amounts of IFN-gamma, whereas CD8(+) cells expressed higher levels of IL-18R and produced more IFN-gamma than CD4(+) cells, Moreover, CD4(-)CD8(-) cells expressed levels of IL-18R comparable to those for CD8(+) cells but produced IFN-gamma one order higher than did CD8(+) cells, These results indicate that the induction of IL-18R and IL-18 responsiveness by IL-12 represents a mechanism underlying enhanced IFN-gamma production by resting T cells, but the operation of this mechanism differs depending on the T cell subset stimulated.

  • 出版日期1998-4-15