Expression of CD57 defines replicative senescence and antigen-induced apoptotic death of CD8+ T cells.
By J. Brenchley, Nitin J. Karandikar, M. Betts, D. Ambrozak, Brenna J. Hill, L. Crotty, J. Casazza, J. Kuruppu, S. Migueles, M. Connors and 3 more. Blood, 2003
1,127 citations recorded by the source corpus.
Subfields: Epidemiology, Immunology
View Paper: https://www.semanticscholar.org/paper/40c93a1db795950858277c1b68e13214b66f43bc
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Citations in the corpus
- Emerging Concepts in the Immunopathogenesis of AIDS (2009, background): “High turnover of CD4 and CD8 T cells imposes a strain on their homeostatic mechanisms (13), resulting in a decrease in the overall halflife of T cells (14), and clonal exhaustion of T cells may ultimately drain memory T cell pools (15, 16).”
- T cell anergy, exhaustion, senescence and stemness in the tumor microenvironment (2013, background): “In addition to low expression of CD28, high expression of Tim-3, CD57, killer cell lectin-like receptor subfamily G, member 1 (KLRG-1) are thought to be associated with T cell senescence [40,60,61 ,62,63 ,64] (Figure 2).”
- Phenotype and function of human T lymphocyte subsets: Consensus and issues (2008, background): “Of note, the expression of CD57 on the cell surface shows a strong relationship with telomere length, in that CD571 T cells have the shortest telomeres (18,32)—implying that these cells have divided the most and have the least proliferative potential amongst the T cell subsets.”
- Seventeen-colour flow cytometry: unravelling the immune system (2004, background): “Ideal markers for immunophenotyping are proteins that are likely to be relevant in the life cycle of a cell type, such as the lymph-node homing molecules CD62L and CCR7 for naive T cell”
- T Cells Genetically Modified to Express an Anti-B-Cell Maturation Antigen Chimeric Antigen Receptor Cause Remissions of Poor-Prognosis Relapsed Multiple Myeloma. (2018, background): “CD57 is another marker of T-cell senescence that has been shown to be an indicator of limited T-cell proliferative capacity.(38,39) The fraction of both CD4 and CD8 CAR-BCMA T cells expressing CD57 increased after infusion, but the magnitude of increase was greater for CD8 T cells (Fig 4C).”
- Immune activation and inflammation in HIV‐1 infection: causes and consequences (2008, background): “These subpopulations tend to lose the capacity to produce IL-2 and present a decline of their proliferative capacity, associated with a shortening of telomere lengths, so that highly differentiated cells (CD28−/CD57+) have been considered as approaching end-stage senescent cells [40,68].”
- Mapping the Diversity of Follicular Helper T Cells in Human Blood and Tonsils Using High-Dimensional Mass Cytometry Analysis. (2015, background): “Interestingly, CD57 expression is often associated with T cell exhaustion and senescence (Brenchley et al., 2003; Wood et al., 2009), but two studies found that CD57+ TFH cells were highly capable of helping B cells (Kim et al., 2001, 2005; Rasheed et al., 2006).”
- PD-1 is a regulator of virus-specific CD8+ T cell survival in HIV infection (2006, background): “Since IL-2 cannot overcome the proliferative defect in CD57+CD8+ T cells ( 45 ), it is of particular interest to examine whether manipulation of PD-1–induced pathways could specifi cally restore their proliferative capacity.”