Two separate mechanisms of enforced viral replication balance innate and adaptive immune activation.
Shaabani, Namir; Khairnar, Vishal; Duhan, Vikas; Zhou, Fan; Tur, Rita Ferrer; Häussinger, Dieter; Recher, Mike; Tumanov, Alexei V; Hardt, Cornelia; Pinschewer, Daniel; Christen, Urs; Lang, Philipp A; Honke, Nadine; Lang, Karl S.
; 67: 82-89, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-26553386
Single-cell RNA-seq reveals TOX as a key regulator of CD8<sup>+</sup> T cell persistence in chronic infection.
Liver-Resident NK Cells Control Antiviral Activity of Hepatic T Cells via the PD-1-PD-L1 Axis.
The transcription factor c-Myb regulates CD8<sup>+</sup> T cell stemness and antitumor immunity.
Production of IL-10 by CD4(+) regulatory T cells during the resolution of infection promotes the maturation of memory CD8(+) T cells.
Subsets of exhausted CD8<sup>+</sup> T cells differentially mediate tumor control and respond to checkpoint blockade.
T cells maintain an exhausted phenotype after antigen withdrawal and population reexpansion.
Effector CD8 T cells dedifferentiate into long-lived memory cells.
Global lymphoid tissue remodeling during a viral infection is orchestrated by a B cell-lymphotoxin-dependent pathway.
A deficiency in nucleoside salvage impairs murine lymphocyte development, homeostasis, and survival.
NK cells negatively regulate CD8 T cells via natural cytotoxicity receptor (NCR) 1 during LCMV infection.