Autophagy is essential for effector CD8(+) T cell survival and memory formation.
Xu, Xiaojin; Araki, Koichi; Li, Shuzhao; Han, Jin-Hwan; Ye, Lilin; Tan, Wendy G; Konieczny, Bogumila T; Bruinsma, Monique W; Martinez, Jennifer; Pearce, Erika L; Green, Douglas R; Jones, Dean P; Virgin, Herbert W; Ahmed, Rafi.
; 15(12): 1152-61, 2014 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-25362489
T Cells in Nonlymphoid Tissues Give Rise to Lymph-Node-Resident Memory T Cells.
Natural Genetic Variation Reveals Key Features of Epigenetic and Transcriptional Memory in Virus-Specific CD8 T Cells.
Local Cellular and Cytokine Cues in the Spleen Regulate In Situ T Cell Receptor Affinity, Function, and Fate of CD8<sup>+</sup> T Cells.
T cells maintain an exhausted phenotype after antigen withdrawal and population reexpansion.
Autophagy-independent functions of UVRAG are essential for peripheral naive T-cell homeostasis.
Aging of Antiviral CD8<sup>+</sup> Memory T Cells Fosters Increased Survival, Metabolic Adaptations, and Lymphoid Tissue Homing.
Production of IL-10 by CD4(+) regulatory T cells during the resolution of infection promotes the maturation of memory CD8(+) T cells.
CD8<sup>+</sup> T Cell Priming in Established Chronic Viral Infection Preferentially Directs Differentiation of Memory-like Cells for Sustained Immunity.
The transcription factor c-Myb regulates CD8<sup>+</sup> T cell stemness and antitumor immunity.
IL-2 is required for the generation of viral-specific CD4<sup>+</sup> Th1 tissue-resident memory cells and B cells are essential for maintenance in the lung.