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CD40L signaling from CD8+ T cells confers protection against influenza infection

CD40L is a principal mediator of a large range of humoral and cellular responses and CD40L-mediated licensing of dendritic cells is known to be necessary for the generation of robust effector and memory CD8+ T cell responses. Although the effects of CD40L when expressed on CD4+ T cells are well stud...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2016-05, Vol.196 (1_Supplement), p.56-56.8
Main Authors: Tay, Neil Q, Lee, Debbie C P, Chua, Yen Leong, Prabhu, Nayana, Kemeny, David Michael
Format: Article
Language:English
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Summary:CD40L is a principal mediator of a large range of humoral and cellular responses and CD40L-mediated licensing of dendritic cells is known to be necessary for the generation of robust effector and memory CD8+ T cell responses. Although the effects of CD40L when expressed on CD4+ T cells are well studied, its role when expressed on CD8+ T cells remain unclear. We have previously reported that CD40L signaling mediates the induction of IL-12 p70 production in dendritic cells when expressed by CD8+ T cells. However, the role and importance of this mechanism in CD8+ T cell responses during an infection are not known. To investigate the function of CD40L when expressed on CD8+ T cells in an in vivo mouse model, we crossed OT-I CD8+ T cell receptor transgenic mice with CD40L−/− mice to generate OVA-specific CD8+ T cells that are unable to expressed CD40L. By transferring CD8+ T cells from these mice into CD40L-competent mice and using a strain of influenza that expresses the OVA epitope recognized by OT-I CD8+ T cells, we were able to create an influenza mouse model where CD40L signaling is absent only on the responding CD8+ T cells. Our analysis indicates that CD40L signaling by CD8+ T cells confers protection against influenza infection and that this is likely dependent on the ability of CD8+ T cells to induce IL-12 p70 production in a CD40L-dependent manner.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.196.Supp.56.8