Card9 controls Dectin-1-induced T-cell cytotoxicity and tumor growth in mice
Haas T, Heidegger S, Wintges A, Bscheider M, Bek S, Fischer JC, Eisenkolb G, Schmickl M, Spoerl S, Peschel C, Poeck H, Ruland J (2017)
Publication Type: Journal article
Publication year: 2017
Journal
Book Volume: 47
Pages Range: 872-879
Journal Issue: 5
Abstract
Activation of the C-type lectin receptor Dectin-1 by β-glucans triggers multiple signals within DCs that result in activation of innate immunity. While these mechanisms can potently prime CD8+ cytotoxic T-cell (CTL) responses without additional adjuvants, the Dectin-1 effector pathways that control CTL induction remain unclear. Here we demonstrate that Dectin-1-induced CTL cross-priming in mice does not require inflammasome activation but strictly depends on the adapter protein Card9 in vitro. In vivo, Dectin-1-mediated Card9 activation after vaccination drives both expansion and activation of Ag-specific CTLs, resulting in long-lasting CTL responses that are sufficient to protect mice from tumor challenge. This Dectin-1-induced antitumor immune response was independent of NK cell function and completely abrogated in Card9-deficient mice. Thus, our results demonstrate that Dectin-1-triggered Card9 signaling but not inflammasome activation can potently cross-prime Ag-specific CTLs, suggesting that this pathway would be a candidate for immunotherapy and vaccine development.
Involved external institutions
Germany (DE)How to cite
APA:
Haas, T., Heidegger, S., Wintges, A., Bscheider, M., Bek, S., Fischer, J.C.,... Ruland, J. (2017). Card9 controls Dectin-1-induced T-cell cytotoxicity and tumor growth in mice. European Journal of Immunology, 47(5), 872-879. https://dx.doi.org/10.1002/eji.201646775
MLA:
Haas, Tobias, et al. "Card9 controls Dectin-1-induced T-cell cytotoxicity and tumor growth in mice." European Journal of Immunology 47.5 (2017): 872-879.
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