期刊
JOURNAL OF IMMUNOLOGY
卷 178, 期 5, 页码 2844-2852出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.178.5.2844
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Stimulation of CD40 on APCs through CD40L expressed on helper CD4(+) T cells activates and licenses the APCs to prime CD8(+) T cell responses. Although other stimuli, such as TLR agonists, can also activate APCs, it is unclear to what extent they can replace the signals provided by CD40-CD40L interactions. In this study, we used an adoptive transfer system to re-examine the role of CD40 in the priming of naive CD8(+) T cells. We find an similar to 50% reduction in expansion and cytokine production in TCR-transgenic T cells in the absence of CD40 on all APCs, and on dendritic cells in particular. Moreover, CD40-deficient and CD40L-deficient mice fail to develop endogenous CTL responses after immunization. Surprisingly, the role for CD40 and CD40L are observed even in the absence of CD4(+) T cells; in this situation, the CD8(+) T cell itself provides CD40L. Furthermore, we show that although TLR stimulation improves T cell responses, it cannot fully substitute for CD40. Altogether, these results reveal a direct and unique role for CD40L on CD8(+) T cells interacting with CD40 on APCs that affects the magnitude and quality of CD8(+) T cell responses.
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