Chapter 2 Natural Killer Cell Tolerance

Jonsson, Helena; Yokoyama, Wayne M.

doi:10.1016/s0065-2776(08)01002-x

Cited by 123 publications

(43 citation statements)

References 212 publications

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“…They also begin to express other NK-associated markers such as NKp46, NK1.1 (in C57B/6 or C57BL/10 mice), CD94, and CD27 [35]. The exact mechanisms of NK maturation have not yet been well-delineated, though licensing of these cells through the ligation of MHCI with NK inhibitory receptors such as the Ly49 and KIR families is required [44]. Without MHCI contact, immature NK cells remain anergic and nonfunctional, explaining why MHCI-deficient mice do not undergo massive inflammation despite having normal numbers of NK cells [44, 45].…”

Section: Introductionmentioning

confidence: 99%

Natural killer cells in inflammatory heart disease

Ong

Rose

Čiháková

2017

Clinical Immunology

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Despite of a multitude of excellent studies, the regulatory role of natural killer (NK) cells in the pathogenesis of inflammatory cardiac disease is greatly underappreciated. Clinical abnormalities in the numbers and functions of NK cells are observed in myocarditis and inflammatory dilated cardiomyopathy (DCMi) as well as in cardiac transplant rejection [1–6]. Because treatment of these disorders remains largely symptomatic in nature, patients have little options for targeted therapies [7, 8]. However, blockade of NK cells and their receptors can protect against inflammation and damage in animal models of cardiac injury and inflammation. In these models, NK cells suppress the maturation and trafficking of inflammatory cells, alter the local cytokine and chemokine environments, and induce apoptosis in nearby resident and hematopoietic cells [1, 9, 10]. This review will dissect each protective mechanism employed by NK cells and explore how their properties might be exploited for their therapeutic potential.

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Section: Introductionmentioning

confidence: 99%

Natural killer cells in inflammatory heart disease

Ong

Rose

Čiháková

2017

Clinical Immunology

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“…Intratumoral NK cells were found to express markedly lower levels of killer-cell immunoglobulin-like receptor (KIR) in comparison to peripheral blood NK cells from the same patients [21, 22]. Tumor-infiltrating NK cells without KIR expression, as non-educated cells, have no cytotoxic capacity [23, 24]. Recent studies also indicated that the phenotype of tumor-infiltrating NK cells without KIR expression was characteristic of immature and nonfunctional NK cells [25].…”

Section: Introductionmentioning

confidence: 99%

Progressive changes in composition of lymphocytes in lung tissues from patients with non-small-cell lung cancer

et al. 2016

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Immune cell infiltration is a common feature of many human solid tumors. Innate and adaptative immune systems contribute to tumor immunosurveillance. We investigated whether tumors evade immune surveillance by inducing states of tolerance and/or through the inability of some immune subpopulations to effectively penetrate tumor nests. Immunohistochemistry and flow cytometry analysis were used to study the composition and distribution of immune subpopulations in samples of peripheral blood, tumor tissue (TT), adjacent tumor tissue (ATT), distant non-tumor tissue (DNTT), cancer nests, cancer stroma, and invasive margin in 61 non-small-cell lung cancer (NSCLC) patients. A significantly higher percentage of T and B cells and significantly lower percentage of NK cells were detected in TT than in DNTT. Memory T cells (CD4+CD45RO+, CD8+CD45RO+) and activated T cells (CD8+DR+) were more prevalent in TT. Alongside this immune activation, the percentage of T cells with immunosuppressive activity was higher in TT than in DNTT. B- cells were practically non-existent in tumor nests and were preferentially located in the invasive margin. The dominant NK cell phenotype in peripheral blood and DNTT was the cytotoxic phenotype (CD56+ CD16+), while the presence of these cells was significantly decreased in ATT and further decreased in TT. Finally, the immunologic response differed between adenocarcinoma and squamous cell carcinoma and according to the tumor differentiation grade. These findings on the infiltration of innate and adaptative immune cells into tumors contribute to a more complete picture of the immune reaction in NSCLC.

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“…Although KIR and HLA class I are encoded on separate chromosomes, a licensing process that is thought to occur during NK cell maturation in the BM protects against the circulation of autoreactive cytotoxic NK cells. 3 Applied to the scenario of allogeneic hematopoietic SCT, certain mismatches at HLA-B and HLA-C loci would be expected to result in circulation of donor-derived NK cells bearing KIR with no compatible ligand on recipient cells, creating the potential for NK cell-mediated alloreactivity in the GVH direction. Such KIR ligand incompatibility can predict the presence of alloreactive NK cells in transplant recipients.…”

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confidence: 99%