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Title: Type 1 conventional CD103+ dendritic cells control effector CD8+ T cell migration, survival, and memory responses during influenza infection
Authors: Ng, See Liang
Teo, Yi Juan
Setiagani, Yolanda Aphrilia
Karjalainen, Klaus
Ruedl, Christiane
Keywords: Influenza
DRNTU::Science::Biological sciences
Dendritic Cell
Issue Date: 2018
Source: Ng, S. L., Teo, Y. J., Setiagani, Y. A., Karjalainen, K., & Ruedl, C. (2018). Type 1 conventional CD103+ dendritic cells control effector CD8+ T cell migration, survival, and memory responses during influenza infection. Frontiers in Immunology, 9, 3043-. doi:10.3389/fimmu.2018.03043
Series/Report no.: Frontiers in Immunology
Abstract: Type 1 conventional CD103+ dendritic cells (cDC1) contribute significantly to the cytotoxic T lymphocyte (CTL) response during influenza virus infection; however, the mechanisms by which cDC1s promote CTL recruitment and viral clearance are unclear. We demonstrate that cDC1 ablation leads to a deficient influenza-specific primary CD8+ T cell response alongside severe pulmonary inflammation, intensifying susceptibility to infection. The diminished pulmonary CTL population is not only a consequence of reduced priming in the lymph node (LN), but also of dysregulated CD8+ T cell egression from the LN and reduced CD8+ T cell viability in the lungs. cDC1s promote S1PR expression on CTLs, a key chemokine receptor facilitating CTL LN egress, and express high levels of the T cell survival cytokine, IL-15, to support CTL viability at the site of infection. Moreover, cDC1 ablation leads to severe impairment of CD8+ T cell memory recall and cross-reactive protection, suggesting that cDC1 are not only involved in primary T cell activation, but also in supporting the development of effective memory CD8+ T cell precursors. Our findings demonstrate a previously unappreciated and multifaceted role of CD103+ DCs in controlling pulmonary T cell-mediated immune responses.
DOI: 10.3389/fimmu.2018.03043
Rights: © 2018 Ng, Teo, Setiagani, Karjalainen and Ruedl. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Fulltext Permission: open
Fulltext Availability: With Fulltext
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