tetano
Editor, Senior Moderator
Immunity. 2016 Sep 24. pii: S1074-7613(16)30343-0. doi: 10.1016/j.immuni.2016.08.019. [Epub ahead of print]
[h=1]Optimal Generation of Tissue-Resident but Not Circulating Memory T Cells during Viral Infection Requires Crosspriming by DNGR-1+ Dendritic Cells.[/h] Iborra S[SUP]1[/SUP], Mart?nez-L?pez M[SUP]2[/SUP], Khouili SC[SUP]2[/SUP], Enamorado M[SUP]2[/SUP], Cueto FJ[SUP]3[/SUP], Conde-Garrosa R[SUP]2[/SUP], Del Fresno C[SUP]2[/SUP], Sancho D[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Despite the crucial role of tissue-resident memory T (Trm) cells in protective immunity, their priming remains poorly understood. Here, we have shown differential priming requirements for Trm versus circulating memory CD8[SUP]+[/SUP] T cells. In vaccinia cutaneous-infected mice, DNGR-1-mediated crosspresentation was required for optimal Trm cell priming but not for their skin differentiation or for circulating memory T cell generation. DNGR-1[SUP]+[/SUP] dendritic cells (DCs) promoted T-bet transcription-factor induction and retention of CD8[SUP]+[/SUP] T cells in the lymph nodes (LNs). Inhibition of LN egress enhanced Trm cell generation, whereas genetic or antibody blockade of DNGR-1 or specific signals provided during priming by DNGR-1[SUP]+[/SUP] DCs, such as interleukin-12 (IL-12), IL-15, or CD24, impaired Trm cell priming. DNGR-1 also regulated Trm cell generation during influenza infection. Moreover, protective immunity depended on optimal Trm cell induction by DNGR-1[SUP]+[/SUP] DCs. Our results reveal specific priming requirements for CD8[SUP]+[/SUP] Trm cells during viral infection and vaccination.
Copyright ? 2016 Elsevier Inc. All rights reserved.
PMID: 27692611 DOI: 10.1016/j.immuni.2016.08.019
[PubMed - as supplied by publisher]
[h=1]Optimal Generation of Tissue-Resident but Not Circulating Memory T Cells during Viral Infection Requires Crosspriming by DNGR-1+ Dendritic Cells.[/h] Iborra S[SUP]1[/SUP], Mart?nez-L?pez M[SUP]2[/SUP], Khouili SC[SUP]2[/SUP], Enamorado M[SUP]2[/SUP], Cueto FJ[SUP]3[/SUP], Conde-Garrosa R[SUP]2[/SUP], Del Fresno C[SUP]2[/SUP], Sancho D[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Despite the crucial role of tissue-resident memory T (Trm) cells in protective immunity, their priming remains poorly understood. Here, we have shown differential priming requirements for Trm versus circulating memory CD8[SUP]+[/SUP] T cells. In vaccinia cutaneous-infected mice, DNGR-1-mediated crosspresentation was required for optimal Trm cell priming but not for their skin differentiation or for circulating memory T cell generation. DNGR-1[SUP]+[/SUP] dendritic cells (DCs) promoted T-bet transcription-factor induction and retention of CD8[SUP]+[/SUP] T cells in the lymph nodes (LNs). Inhibition of LN egress enhanced Trm cell generation, whereas genetic or antibody blockade of DNGR-1 or specific signals provided during priming by DNGR-1[SUP]+[/SUP] DCs, such as interleukin-12 (IL-12), IL-15, or CD24, impaired Trm cell priming. DNGR-1 also regulated Trm cell generation during influenza infection. Moreover, protective immunity depended on optimal Trm cell induction by DNGR-1[SUP]+[/SUP] DCs. Our results reveal specific priming requirements for CD8[SUP]+[/SUP] Trm cells during viral infection and vaccination.
Copyright ? 2016 Elsevier Inc. All rights reserved.
PMID: 27692611 DOI: 10.1016/j.immuni.2016.08.019
[PubMed - as supplied by publisher]