摘要

Type I IFN and IL-12 are well documented to serve as so called "signal 3" cytokines, capable of facilitating CD8(+) T cell proliferation, effector function and memory formation. While their ability to serve in this capacity is well established, to date, no non-cytokine signal 3 mediators have been clearly identified. We have established a vaccine model system in which the primary CD8(+) T cell response is independent of either IL-12 or type I IFN receptors, but dependent on CD27/CD70 interactions. We show here that primary and secondary CDS+ T cell responses are generated in the combined deficiency of IFN and IL-12 signaling. In contrast, antigen specific CD8(+) T cell responses are compromised in the absence of the TNF receptors CD27 and 0X40. These data

  • 出版日期2012-2-1