Signals required for programming effector and memory development by CD8+ T cells

By M. Mescher, Julie M. Curtsinger, P. Agarwal, K. Casey, Michael Y. Gerner, Christopher D. Hammerbeck, Flavia E. Popescu, Zhengguo Xiao. Immunological Reviews, 2006

676 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/ebdbd3fe3d64f6a82f553abae2ce55850ca98161

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. M. Bevan
2. E. Wherry
3. V. Badovinac
4. J. Harty
5. S. Kaech
6. W. Cui
7. Laura M. McLane
8. Mohamed S. Abdel-Hakeem

Citations in the corpus

• Virus-specific T cells engineered to coexpress tumor-specific receptors: persistence and antitumor activity in individuals with neuroblastoma (2008, background): “By contrast, when virus-infected B cells engage EBV-CTLs through their native receptor, a panoply of physiological co-stimulation follow”
• Redefining chronic viral infection. (2009, neutral): “In addition to influencing CD8 T cell activation and expansion (Mescher et al., 2006), IL-12, IFN-αβ, and other inflammatory signals shape T cell memory.”
• CD8+ T Cells: Foot Soldiers of the Immune System (2011, neutral): “Use of a bicistronic reporter mouse strain Ifng-YFP to visualize activation of the gene encoding interferon (IFN)- g reveals that the YFP signal is turned on within 24 hr of DC-peptide immunization (Beuneu et al., 2010).”
• Inflammatory Cytokines as a Third Signal for T Cell Activation (2010, neutral): “TCR and costimulatory signals initiate proliferation of naïve cells, but in the absence of a specific cytokine signal the cells fail to develop optimal effector functions, survive poorly, and do not form a responsive memory population [1].”
• Structural design of engineered costimulation determines tumor rejection kinetics and persistence of CAR T cells (2015, neutral): “…regulate genes involved in CTL function by sustaining the expression of T-bet and Eomes as well as through chromatin remodeling (Agarwal et al., 2009; Lim et al., 2014), supporting the acquisition of better effector function (Hervas-Stubbs et al., 2010; Marshall et al., 2010; Mescher et al., 2006).”
• Shaping and reshaping CD8+ T-cell memory (2008, background): “Recent data suggest that signals received during this interaction — including antigen (signal 1), co-stimulation (signal 2), and pro-inflammatory cytokines (signal 3) — programme the responding CD8 + T cells in a fashion that will eventually lead to the formation of memory T-cell population”
• Interleukin-2 and Inflammation Induce Distinct Transcriptional Programs that Promote the Differentiation of Effector Cytolytic T Cells (2010, background): “In different settings, signal 3 has been shown to be crucial for inducing CTL effector functions (Curtsinger et al., 2003; Mescher et al., 2006), for driving antigen-activated CD8 T cells toward a short-lived effector cell fate (Joshi et al.”
• Inflammation directs memory precursor and short-lived effector CD8(+) T cell fates via the graded expression of T-bet transcription factor. (2007, background): “Although exposure to inflammatory cytokines may reduce effector CD8 T cell longevity, signals from IL-12 and type I/II IFNs also play a critical role in enhancing effector CD8 T cell expansion and function (Mescher et al., 2006).”
• CD8 T Cell Exhaustion During Chronic Viral Infection and Cancer. (2019, background): “The general three-signal model (126) of signal 1 from antigen, signal 2 from costimulation or, in this case, negative costimulation by IRs, and signal 3 from inflammation and soluble mediators is a useful framework for discussing the development of T cell exhaustion (Figure 2).”