2017
DOI: 10.1016/j.smim.2017.08.012
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Memory responses of natural killer cells

Abstract: Natural killer (NK) cells have traditionally been classified as a cellular component of the innate immune system, given their ability to rapidly produce effector cytokines and kill infected or transformed cells without prior exposure. More recently, NK cells have been shown to possess features of adaptive immunity such as clonal expansion, longevity, and robust recall responses. NK cell memory can be broadly divided into two categories: antigen-specific and antigen-independent. In the first case, exposure to c… Show more

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Cited by 72 publications
(65 citation statements)
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References 119 publications
(144 reference statements)
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“…It is believed that the newly nascent transformed cells can be initially eliminated by the host immune system based on innate immunity and adaptive immunity, and the destroyed cells then release various tumour antigens, further stimulate adaptive immunity and activate T/B lymphocytes. Studies have shown that tumour lymphatic infiltration and better survivability of patients have a strong correlation, [23][24][25] suggesting that patients F I G U R E 4 Validation of external datasets. A, Expression distribution of 13 immune metagenes in 4 subtypes in the validation set; B, Gene expression score of the tumour stroma scores, the immune scores and the tumour purity in the validation set; C, Expression distribution of 8 immune checkpoint genes in 4 subtypes in the validation set.…”
Section: Discussionmentioning
confidence: 99%
“…It is believed that the newly nascent transformed cells can be initially eliminated by the host immune system based on innate immunity and adaptive immunity, and the destroyed cells then release various tumour antigens, further stimulate adaptive immunity and activate T/B lymphocytes. Studies have shown that tumour lymphatic infiltration and better survivability of patients have a strong correlation, [23][24][25] suggesting that patients F I G U R E 4 Validation of external datasets. A, Expression distribution of 13 immune metagenes in 4 subtypes in the validation set; B, Gene expression score of the tumour stroma scores, the immune scores and the tumour purity in the validation set; C, Expression distribution of 8 immune checkpoint genes in 4 subtypes in the validation set.…”
Section: Discussionmentioning
confidence: 99%
“…CD11b + CD27 À NK cells have been reported to show increased expression of CD62L, S1P 5 (sphingosine-1-phosphate receptor 5), CX 3 CR1, CXCR3, CXCR4 and CCR1. [6][7][8][9] Although both CD25 and CD69 were found only at steady-state levels in S. schenckii-infected mice, KLRG1 had its expression up-regulated more than twofold. Additionally, CX 3 CR1 is highly expressed and mainly found on KLRG1 + NK cells (considered fully mature CD11b + CD27 À cells) identifying an even later maturation stage shown to have impaired IFN-c production and cytotoxicity towards YAC-1 cells under cytokine stimulation.…”
Section: Discussionmentioning
confidence: 99%
“…1,2 NK cell development from the earliest NK cell-committed precursor to functionally competent mature NK cells is a stepwise process that involves the sequential acquisition of a series of surface molecules. [6][7][8][9] However, our current understanding of NK cell biology in disease conditions comes almost entirely from the setting of tumours and viral infections, with data on NK cell modulation by fungal infections being preliminary at best. Additionally, murine NK cells can be further dissected into four distinct maturation stages defined by the differential surface expression of CD11b (a M integrin) and CD27 [a tumour necrosis factor (TNF) receptor family member], from the least to the most mature, as follow: CD11b À CD27 À ?…”
Section: Introductionmentioning
confidence: 99%
“…A number of recent studies have concentrated on defining the extracellular and intracellular requirements for generating robust expansion of MCMV‐specific NK cells. Ly49H ligation (analogous to TCR engagement for T‐cell activation, “signal 1”) is required but not sufficient for optimal proliferation of Ly49H + NK cells, which also need costimulation (“signal 2”) and proinflammatory cytokine signaling (“signal 3”) . NK cell costimulation comes by way of the costimulatory molecule DNAX accessary molecule 1 (DNAM‐1), which interacts with its ligand poliovirus receptor (PVR or CD155) during MCMV infection .…”
Section: Waves Of Antiviral Immunitymentioning
confidence: 99%