Selected Toll-like Receptor Ligands and Viruses Promote Helper-Independent Cytotoxic T Cell Priming by Upregulating CD40L on Dendritic Cells
- Author(s)
- Johnson, S; Zhan, YF; Sutherland, RM; Mount, AM; Bedoui, S; Brady, JL; Carrington, EM; Brown, LE; Belz, GT; Heath, WR; Lew, AM;
- Details
- Publication Year 2009-02-20,Volume 30,Issue #2,Page 218-227
- Journal Title
- IMMUNITY
- Publication Type
- Journal Article
- Abstract
- CD40L (CD154) on CD4(+) T cells has been shown to license dendritic cells (DCs) via CD40 to prime cytotoxic T lymphocyte (CTL) responses. We found that the converse (CD40L on DCs) was also important. Anti-CD40L treatment decreased endogenous CTL responses to both ovalbumin and influenza infection even in the absence of CD4(+) T cells. DCs expressed CD40L upon stimulation with agonists to Toll-like receptor 3 (TLR3) and TLR9. Moreover, influenza infection, which stimulates CTLs without help, upregulated CD40L on DCs, but herpes simplex infection, which elicits CTLs through help, did not. CD40L-deficient (Cd40lg(-/-)) DCs are suboptimal both in vivo in bone marrow chimera experiments and in vitro in mixed lymphocyte reactions. In contrast, Cd40lg(-/-)CD8(+) T cells killed as effectively as wild-type cells. Thus, CD40L upregulation on DCs promoted optimal priming of CD8(+) T cells without CD4(+) T cells, providing a mechanism by which pathogens may elicit helper-independent CTL immunity.
- Publisher
- CELL PRESS
- Keywords
- ANTIVIRAL IMMUNITY; CROSS-PRESENTATION; CD8-T-CELL MEMORY; CD40-CD40 LIGAND; CD4-T-CELL HELP; CUTTING EDGE; TUMOR-CELLS; LYMPH-NODE; IN-VIVO; EXPRESSION
- Publisher's Version
- https://doi.org/10.1016/j.immuni.2008.11.015
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- Refer to copyright notice on published article.
Creation Date: 2009-02-20 12:00:00