Neutrophils Induced Licensing of Natural Killer Cells

Amano, Keishiro; Hirayama, Masahiro; Azuma, Eiichi; Iwamoto, Shotaro; Keida, Yoshitaka; Komada, Yoshihiro

doi:10.1155/2015/747680

Cited by 17 publications

(18 citation statements)

References 22 publications

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“…It is well known that the number and functions of NK cells depend on the cytokine environment and on cell-to-cell interactions with myeloid cells such as monocytes, macrophages, and neutrophils (22)(23)(24)(25)(26)(27). We, therefore, monitored myeloid populations in the lung in response to metastasis induction (gating strategies in Supplementary Fig.…”

Section: M1-like Myeloid Cells Accumulate In the Lungs Of Primary Tummentioning

confidence: 99%

Primary Tumors Limit Metastasis Formation through Induction of IL15-Mediated Cross-Talk between Patrolling Monocytes and NK Cells

Kubo

Mensurado

Gonçalves-Sousa

et al. 2017

Cancer Immunology Research

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Metastases are responsible for the vast majority of cancerrelated deaths. Although tumor cells can become invasive early during cancer progression, metastases formation typically occurs as a late event. How the immune response to primary tumors may dictate this outcome remains poorly understood, which hampers our capacity to manipulate it therapeutically. Here, we used a twostep experimental model, based on the highly aggressive B16F10 melanoma, that temporally segregates the establishment of primary tumors (subcutaneously) and the formation of lung metastases (from intravenous injection). This allowed us to identify a protective innate immune response induced by primary tumors that inhibits experimental metastasis. We found that in the presence of primary tumors, increased numbers of natural killer (NK) cells with enhanced IFNg, granzyme B, and perforin production were recruited to the lung upon metastasis induction. These changes were mirrored by a local accumulation of patrolling monocytes and macrophages with high expression of MHC class II and NOS2. Critically, the protective effect on metastasis was lost upon patrolling monocyte or NK cell depletion, IL15 neutralization, or IFNg ablation. The combined analysis of these approaches allowed us to establish a hierarchy in which patrolling monocytes, making IL15 in response to primary tumors, activate NK cells and IFNg production that then inhibit lung metastasis formation. This work identifies an innate cell network and the molecular determinants responsible for "metastasis immunosurveillance," providing support for using the key molecular mediator, IL15, to improve immunotherapeutic outcomes.

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Section: M1-like Myeloid Cells Accumulate In the Lungs Of Primary Tummentioning

confidence: 99%

Primary Tumors Limit Metastasis Formation through Induction of IL15-Mediated Cross-Talk between Patrolling Monocytes and NK Cells

Kubo

Mensurado

Gonçalves-Sousa

et al. 2017

Cancer Immunology Research

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“…Besides producing cytokines and chemokines, another novel and emerging aspect consists in the ability of neutrophils to interact with, and modulate the activity of different leukocyte types in vitro and in vivo. Recent studiesalso highlight a new role for neutrophils as nonredundant regulatory cells ensuring the terminal maturation of NK cells in both humans and mice [58][59][60] . Future studies in natural hosts will help to decipher to which extent these functions play a role in the pathogenic outcome of HIV/SIV infections.…”

Section: Polymorphonuclear Cellsmentioning

confidence: 99%

Innate immune cell responses in non pathogenic versus pathogenic SIV infections

Huot

Rascle

García-Téllez

et al. 2016

Current Opinion in Virology

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HIV-1/SIVmac infections deeply disturb innate host responses. Most studies have focused on the impact on dendritic cells and NK cells. A few but insufficient data are available on other innate immune cell types, such as neutrophils. It has been shown that innate lymphoid cells are depleted early and irreversibly during SIVmac/HIV-1 infections. Studies in natural hosts of SIV have contributed to pinpoint that early control of inflammation is crucial. In natural hosts, plasmacytoid dendritic cells, myeloid dendritic cells and NK cells are depleted during acute infection but return to normal levels by the end of acute infection. We summarize here the similarities and differences of various types of innate immune responses in natural hosts compared to pathogenic HIV/SIV mac infections.

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“… showed that Genista mice, which lack mature neutrophils, displayed a normal Ly49 repertoire despite an alteration in NK cell function. Recent data provide an opposing view . Accessory cells likely influence NK cell development and maturation by means of cytokines, in particular IL‐15 .…”

Section: The Useful the Dangerous And The Useless: A Positive Selecmentioning

confidence: 99%

Selection, tuning, and adaptation in mouse NK cell education

Kadri

Thanh

Höglund

2015

Immunological Reviews

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Natural killer (NK) cells recognize transformed cells with an array of germline-encoded inhibitory and activating receptors. Inhibitory Ly49 receptors bind major histocompatibility complex class I (MHC-I) molecules, providing a mechanism by which NK cells maintain self-tolerance yet eliminate cells expressing reduced levels of MHC-I. Additionally, MHC-I molecules are required for NK cell education, a process in which NK cells acquire responsiveness. In this review, we discuss three facets of MHC class I-dependent education of mouse NK cells: skewing of the inhibitory receptor repertoire, induction of functional responsiveness, and tuning in response to changes in MHC-I expression. We discuss prevailing models for education such as licensing and disarming and propose a model for positive selection of 'useful' NK cell subsets. Furthermore, we argue that both repertoire skewing and functional NK cell education may be altered in mature NK cells subject to changes in MHC-I input and suggest that this process may provide increased dynamics to the NK cell system.

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Neutrophils Induced Licensing of Natural Killer Cells

Cited by 17 publications

References 22 publications

Primary Tumors Limit Metastasis Formation through Induction of IL15-Mediated Cross-Talk between Patrolling Monocytes and NK Cells

Primary Tumors Limit Metastasis Formation through Induction of IL15-Mediated Cross-Talk between Patrolling Monocytes and NK Cells

Innate immune cell responses in non pathogenic versus pathogenic SIV infections

Selection, tuning, and adaptation in mouse NK cell education

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