Toll-Like Receptors in Natural Killer Cells and Their Application for Immunotherapy

Noh, Jin-Yong; Yoon, Suk Ran; Kim, Tae-Don; Choi, In Pyo; Jung, Hye Young

doi:10.1155/2020/2045860

Cited by 60 publications

(52 citation statements)

References 101 publications

(126 reference statements)

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“…The innate immune system is the first barrier for human self-protection that activates nonspecific immune cells to respond to pathogens [ 18 ], and immune cells are restricted to enter into the vascular endothecium under normal physiological conditions [ 19 ]. The intimal lipid particles in the artery wall promote the production of selectins, monocyte chemoattractant protein-1 (MCP-1), and vascular cell adhesion molecule-1 (VCAM-1) in endothelial cells, which provide monocytes and other inflammatory cells with specific stimuli and anchors [ 15 , 19 ].…”

Section: Immune and Inflammation In The Pathogenesis Of Acsmentioning

confidence: 99%

Immune and Inflammation in Acute Coronary Syndrome: Molecular Mechanisms and Therapeutic Implications

Wang

Liu

Shao

et al. 2020

Journal of Immunology Research

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Acute coronary syndrome (ACS) is a major cause of acute death worldwide. Both innate and adaptive immunity regulate atherosclerosis progression, plaque stability, and thrombus formation. Immune and inflammation dysfunction have been indicated in the pathogenesis of ACS. The imbalance in the proatherogenic and antiatherogenic immune networks promotes the transition of plaques from a stable to unstable state and results in the occurrence of acute coronary events. The residual inflammatory risk (RIR) has received increasing attention in recent years, and lowering RIR has been expected to improve the outcomes of ACS patients. The CANTOS, COLCOT, and LoDoCo trials verified the benefits of reducing cardiovascular events using anti-inflammation therapies; however, most of the other studies focusing on lowering RIR produced negative or contradicting results. Therefore, restoring the balance in autoimmune regulation is essential because proatherogenic and antiatherogenic immunomodulatory effects are equally important in the complex human immune network. In this review, we summarized the recent evidence of the roles of proatherogenic and antiatherogenic immune networks in the pathogenesis of ACS and discussed how immune and inflammation contribute to atherosclerosis progression, plaque instability, and adverse cardiovascular events. We also provide a “from bench to bedside” perspective of a novel and promising personalized strategy in RIR intervention and therapeutic approaches for the treatment of ACS.

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Section: Immune and Inflammation In The Pathogenesis Of Acsmentioning

confidence: 99%

Immune and Inflammation in Acute Coronary Syndrome: Molecular Mechanisms and Therapeutic Implications

Wang

Liu

Shao

et al. 2020

Journal of Immunology Research

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“…The activation of innate immune receptors as Toll-like receptors (TLRs) and nucleotide oligomerization domain-like receptors (NLRs) induces innate-immunity-mediated autophagy upregulation (150)(151)(152). TLRs interact with pathogens on the cell surface and usually are also expressed in cancer cells, inducing cytokines production together with NF-kB and MAPK pathways activation (151)(152)(153). TLRs are proposed to activate autophagy as demonstrated for TLR2 that enhances innate immunity through ERK and JNK signaling pathways after autophagy stimulation, and also boosts autophagy in glioma cells being correlated with poorer patients outcome (154,155).…”

Section: Autophagy and Innate Immunitymentioning

confidence: 99%

Emerging Autophagy Functions Shape the Tumor Microenvironment and Play a Role in Cancer Progression - Implications for Cancer Therapy

et al. 2020

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The tumor microenvironment (TME) is a complex environment where cancer cells reside and interact with different types of cells, secreted factors, and the extracellular matrix. Additionally, TME is shaped by several processes, such as autophagy. Autophagy has emerged as a conserved intracellular degradation pathway for clearance of damaged organelles or aberrant proteins. With its central role, autophagy maintains the cellular homeostasis and orchestrates stress responses, playing opposite roles in tumorigenesis. During tumor development, autophagy also mediates autophagy-independent functions associated with several hallmarks of cancer, and therefore exerting several effects on tumor suppression and/or tumor promotion mechanisms. Beyond the concept of degradation, new different forms of autophagy have been described as modulators of cancer progression, such as secretory autophagy enabling intercellular communication in the TME by cargo release. In this context, the synthesis of senescence-associated secretory proteins by autophagy lead to a senescent phenotype. Besides disturbing tumor treatment responses, autophagy also participates in innate and adaptive immune signaling. Furthermore, recent studies have indicated intricate crosstalk between autophagy and the epithelial-mesenchymal transition (EMT), by which cancer cells obtain an invasive phenotype and metastatic potential. Thus, autophagy in the cancer context is far broader and complex than just a cell energy sensing mechanism. In this scenario, we will discuss the key roles of autophagy in the TME and surrounding cells, contributing to cancer development and progression/EMT. Finally, the potential intervention in autophagy processes as a strategy for cancer therapy will be addressed.

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“…Thus, the activation program of NK cells derives from the integration of activator and inhibitor signals, which varies according to the nature of the interacting cells. In addition, NK cells also express cytokines and chemokines receptors that are crucial for the regulation of NK cell functions and Toll like receptors that mediate the production of IFN-g and increase cytotoxicity (15).…”

Section: Phenotype Maturation Cytotoxic Activity and Distribution mentioning

confidence: 99%

The Role of Natural Killer Cells in the Immune Response in Kidney Transplantation

et al. 2020

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Natural killer cells (NK) represent a population of lymphocytes involved in innate immune response. In addition to their role in anti-viral and anti-tumor defense, they also regulate several aspects of the allo-immune response in kidney transplant recipients. Growing evidence suggests a key role of NK cells in the pathogenesis of immune-mediated graft damage in kidney transplantation. Specific NK cell subsets are associated with operational tolerance in kidney transplant patients. On the other side, allo-reactive NK cells are associated with chronic antibody-mediated rejection and graft loss. Moreover, NK cells can prime the adaptive immune system and promote the migration of other immune cells, such as dendritic cells, into the graft leading to an increased allo-immune response and, eventually, to chronic graft rejection. Finally, activated NK cells can infiltrate the transplanted kidney and cause a direct graft damage. Interestingly, immunosuppression can influence NK cell numbers and function, thus causing an increased risk of post-transplant neoplasia or infection. In this review, we will describe how these cells can influence the innate and the adaptive immune response in kidney transplantation and how immunosuppression can modulate NK behavior.

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Toll-Like Receptors in Natural Killer Cells and Their Application for Immunotherapy

Cited by 60 publications

References 101 publications

Immune and Inflammation in Acute Coronary Syndrome: Molecular Mechanisms and Therapeutic Implications

Immune and Inflammation in Acute Coronary Syndrome: Molecular Mechanisms and Therapeutic Implications

Emerging Autophagy Functions Shape the Tumor Microenvironment and Play a Role in Cancer Progression - Implications for Cancer Therapy

The Role of Natural Killer Cells in the Immune Response in Kidney Transplantation

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