Effector and memory CTL differentiation.

By Matthew A. Williams, M. Bevan. Annual Review of Immunology, 2007

1,011 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/f689c3ae9b1ce3850ec0a845a961d30cc4ada988

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. Rafi Ahmed
2. E. Wherry
3. M. Bevan
4. S. Kaech
5. Joseph C. Sun
6. V. Badovinac
7. J. Harty
8. D. Masopust

Citations in the corpus

• Interleukin-2 Receptor Signaling: At the Interface between Tolerance and Immunity (2010, neutral): “A small proportion survives and persists asmemory Tcells that protect the host long-termagainst reinfection with the same pathogen (Harty and Badovinac, 2008; Williams and Bevan, 2007).”
• T cell exhaustion (2011, background): “T cell responses to acute infections After infections that are cleared acutely, highly functional memory T cells develop and are endowed with several defining properties that distinguish them from naive, effector or other subsets of memory-like T cell”
• Coregulation of CD8+ T cell exhaustion during chronic viral infection by multiple inhibitory receptors (2008, background): “1679" language="eng" relation="no"> After acute viral infection, memory CD8 + T cells rapidly reactivate effector functions, have high proliferative potential and are maintained by antigen-independent homeostatic proliferatio”
• mTOR regulates memory CD8 T cell differentiation (2009, neutral): “Three different treatment periods were used: (1) throughout LCMV infection (day 21 before infection to the memory phase, day 35 post-infection); (2) the T-cell expansion phase (day 21 before infection to day 8 post-infection); or (3) T-cell contraction phase (day 8 to the memory phase, day 35 post-i”
• Prolonged interleukin-2Ralpha expression on virus-specific CD8+ T cells favors terminal-effector differentiation in vivo. (2010, background): “differentiation (Kaech and Ahmed, 2001; Kalia et al., 2006; Mercado et al., 2000; van Stipdonk et al., 2003; van Stipdonk et al., 2001; Williams and Bevan, 2007 ).”
• Differentiation and persistence of memory CD8+ T cells depend on T cell factor 1 (2010, background): “…affected by extracellular stimuli including the strength and timing of stimulatory signals derived from T cell receptor (TCR)antigen interactions, costimulation, and inflammatory cytokines including interferons and IL-12 (Harty and Badovinac, 2008; Kaech and Wherry, 2007; Williams and Bevan, 2007).”
• Tissue-Resident Memory T Cells (2014, background): “…productively primed within SLOs, they give rise to effector cells that migrate throughout the host and leave behind a memory population that persists long after pathogen clearance (Dutton et al., 1998; Harty and Badovinac, 2008; Lefrançois, 2006; Sallusto et al., 2010; Williams and Bevan, 2007).”
• NK cell development, homeostasis and function: parallels with CD8+ T cells (2011, background): “Although this expansion is not as prolific as the several-thousand-fold expansion measured in antigen-specific T cell response”
• Immunological Principles Guiding the Rational Design of Particles for Vaccine Delivery. (2017, neutral): “This cytotoxic/cytolytic ability is crucial in the maintenance of effective immune control against intracellular pathogens and cancer.(38) CD4+ T cells recognize peptides (9-20 amino acids) complexed with MHC class II molecules, which are mainly expressed by professional APCs (i.”
• Interleukin-2 and Inflammation Induce Distinct Transcriptional Programs that Promote the Differentiation of Effector Cytolytic T Cells (2010, background): “CD8 T cell differentiation upon infection is complex and integrates multiple signals including strength of TCR stimulus and costimulation, IL-2R signals, and inflammation (Williams and Bevan, 2007).”
• Heterogeneity and cell-fate decisions in effector and memory CD8+ T cell differentiation during viral infection. (2007, background): “CD4+ T Cell Help and IL-2 CD4+ T cells, CD40-CD40L signals, and IL-2 help to maximize effector CD8+ T cell expansion, an effective E / M transition, and long-term maintenance after acute viral infections (Northrop and Shen, 2004; Rocha and Tanchot, 2004; Williams and Bevan, 2007).”