tetano
Editor, Senior Moderator
Front Immunol. 2018 Dec 21;9:3043. doi: 10.3389/fimmu.2018.03043. eCollection 2018.
[h=1]Type 1 Conventional CD103[SUP]+[/SUP] Dendritic Cells Control Effector CD8[SUP]+[/SUP] T Cell Migration, Survival, and Memory Responses During Influenza Infection.[/h] Ng SL[SUP]1[/SUP], Teo YJ[SUP]1[/SUP], Setiagani YA[SUP]1[/SUP], Karjalainen K[SUP]1[/SUP], Ruedl C[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Type 1 conventional CD103[SUP]+[/SUP] 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[SUP]+[/SUP] 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[SUP]+[/SUP] T cell egression from the LN and reduced CD8[SUP]+[/SUP] 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[SUP]+[/SUP] 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[SUP]+[/SUP] T cell precursors. Our findings demonstrate a previously unappreciated and multifaceted role of CD103[SUP]+[/SUP] DCs in controlling pulmonary T cell-mediated immune responses.
[h=4]KEYWORDS:[/h] CD103; CD8+ T cell; Clec9A; dendritic cell; inflammation; influenza; migration; survival
PMID: 30622538 PMCID: PMC6308161 DOI: 10.3389/fimmu.2018.03043
Free full text
[h=1]Type 1 Conventional CD103[SUP]+[/SUP] Dendritic Cells Control Effector CD8[SUP]+[/SUP] T Cell Migration, Survival, and Memory Responses During Influenza Infection.[/h] Ng SL[SUP]1[/SUP], Teo YJ[SUP]1[/SUP], Setiagani YA[SUP]1[/SUP], Karjalainen K[SUP]1[/SUP], Ruedl C[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Type 1 conventional CD103[SUP]+[/SUP] 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[SUP]+[/SUP] 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[SUP]+[/SUP] T cell egression from the LN and reduced CD8[SUP]+[/SUP] 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[SUP]+[/SUP] 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[SUP]+[/SUP] T cell precursors. Our findings demonstrate a previously unappreciated and multifaceted role of CD103[SUP]+[/SUP] DCs in controlling pulmonary T cell-mediated immune responses.
[h=4]KEYWORDS:[/h] CD103; CD8+ T cell; Clec9A; dendritic cell; inflammation; influenza; migration; survival
PMID: 30622538 PMCID: PMC6308161 DOI: 10.3389/fimmu.2018.03043
Free full text