• Breast cancer
• Cancer therapy
• Candida albicans
• Immune responses
• Tumor progression

• Fas/FasL
• TRAIL/TRAILR
• cytokines
• immunotherapy
• natural killer cells
• ovarian cancer

• Humans
• Female
• Immunotherapy
• Ovarian Neoplasms/therapy
• Killer Cells, Natural
• Antibody-Dependent Cell Cytotoxicity
• Tumor Microenvironment

• Gastric cancer
• Glycolysis
• Immune evasion
• Immunotherapy
• Microenvironment

• 82174197 National Natural Science Foundation of China
• BK20211392 Natural Science Foundation of Jiangsu Province
• LGY2018065 "333" Project of Jiangsu Province
• Y2021RC29 Jiangsu Provincial Hospital of Traditional Chinese Medicine Academic Talent Program
• “333” Project of Jiangsu Province
• A Project Funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions

• CAR-NK
• Cancer treatment
• Clinical trials
• Immunotherapy
• NK cells
• Preclinical studies

• 2016YFC1303403 National Key Research and Development Program of China
• 2020YFC0860200 National Key Research and Development Program of China
• 81972878 National Natural Science Foundation of China
• 82172733 National Natural Science Foundation of China
• 2020YFS0008 the Key Research and Development Program of Sichuan Province

• AML
• BiKEs
• CAR-NK
• TriKEs
• immunotherapy
• natural killer cells

• Humans
• Leukemia, Myeloid, Acute/pathology
• Killer Cells, Natural
• Immunotherapy, Adoptive/methods
• Receptors, KIR/metabolism
• Cytokines/metabolism

• Acute myeloid leukemia
• Hsp70
• Immunotherapy
• Natural Killer Cells
• PD-1

• B-cell lymphoma
• CAR-NK cell
• Lymphoma
• T-cell lymphoma
• chimeric antigen receptor
• immunotherapy
• natural killer cell

• Cancer
• Cellular immunotherapy
• Chimeric antigen receptor
• Natural killer cells
• T cells

The development of chimeric antigen receptor T (CAR-T) cell therapy, a specific type of immunotherapy, in recent decades was a fantastic breakthrough for the treatment of hematological malignancies. However, difficulties in collecting normal T cells from patients and the time cost of manufacturing CAR-T cells have limited the application of CAR-T-cell therapy. In addition, the termination of related clinical trials on universal CAR-T cell therapy has made further research more difficult. Natural killer (NK) cells have drawn great attention in recent years. Chimeric antigen receptor-NK (CAR-NK) cell therapy is a promising strategy in the treatment of malignant tumors because of its lack of potential for causing graft-versus-host disease (GVHD). In this review, we will address the advances in and achievements of CAR-NK cell therapy.

• Humans
• Receptors, Chimeric Antigen
• Immunotherapy, Adoptive
• Killer Cells, Natural
• Neoplasms
• Cell- and Tissue-Based Therapy

• National Natural Science Foundation of China

Bone Marrow Stromal Cell Antigen 2 (BST2) is a type II transmembrane protein expressed on various cell types that tethers the release of viruses. Natural killer (NK) cells express low levels of BST2 under normal conditions but exhibit increased expression of BST2 upon activation. In this study, we show for the first time that murine BST2 can control the cytotoxicity of NK cells. The cytoplasmic tail of murine BST2 contains an immunoreceptor tyrosine-based inhibitory motif (ITIM). The absence of BST2 on NK cells can enhance their cytotoxicity against tumor cells compared to wild type NK cells. NK cells isolated from NZW mice, which express ITIM-deficient BST2, also showed higher cytotoxicity than wild type NK cells. In addition, we found that galectin-8 and galectin-9 were ligands of BST2, since blocking galectin-8 or -9 with monoclonal antibodies enhanced the cytotoxicity of NK cells. These results suggested that BST2 might be a novel NK cell inhibitory receptor as it was involved in regulating NK cell cytotoxicity through its interaction with galectins.

Gastric cancer is one of the most common malignant tumours worldwide, with the fifth and third highest morbidity and mortality, respectively, of all cancers. Survival is limited, as most of the patients are diagnosed at an advanced stage, and are not suitable for surgery with a curative intent. Chemotherapy has only modestly improved patients’ outcomes and is mainly given with a palliative intent. Immunotherapy has improved overall survival of patients with gastric cancer, and has thus become a new standard of care in clinic. In this review we discuss the strong molecular rationale for the administration of immunotherapy in this disease and analyse the clinical data supporting its use.

Gastric cancer has a median survival of 11 months, and this poor prognosis has not improved over the last 30 years. Recent pre-clinical data suggest that there is high tumour-related neoantigen expression in gastric cancer cells, suggesting that a clinical strategy that enhances the host’s immune system against cancer cells may be a successful approach to improve clinical outcomes. Additionally, there has been an increasing amount of translational evidence highlighting the relevance of PD-L1 expression in gastric cancer cells, indicating that PD-1/PD-L1 inhibitors may be useful. Several molecular subgroups of gastric cancer have been identified to respond with excellent outcomes to immunotherapy, including microsatellite instable tumours, tumours bearing a high tumour mutational burden, and tumours related to a chronic EBV infection. In gastric cancer, immunotherapy has produced durable responses in chemo-refractory patients; however, most recently there has been a lot of enthusiasm as several large-scale clinical trials highlight the improved survival noted from the incorporation of immunotherapy in the first line setting for advanced gastric cancer. Our review aims to discuss current pre-clinical and clinical data supporting the innovative role of immunotherapy in gastric cancer.

• bone marrow
• cell–cell interactions
• marrow-infiltrating lymphocytes
• mesenchymal stromal cells
• multiple myeloma

• PI20/00991, CP21/00111 Instituto de Salud Carlos III

• T cells
• breast cancer
• chimeric antigen receptor (CAR)
• immunotherapy
• natural killer (NK) cells

• Breast Neoplasms/metabolism
• Female
• Humans
• Immunotherapy, Adoptive
• Killer Cells, Natural
• Neoplasms/drug therapy
• Receptors, Chimeric Antigen/genetics
• Receptors, Chimeric Antigen/metabolism
• T-Lymphocytes
• Tumor Microenvironment

• CAR
• Cancer
• Chimeric antigen receptor
• Immunotherapy
• NK cell
• Natural killer cells

The emergence of cancer immunotherapies utilizing adoptive cell transfer (ACT) continues to be one of the most promising strategies for cancer treatment. Mast cells (MCs) which occur throughout vascularized tissues, are most commonly associated with Type I hypersensitivity, bind immunoglobin E (IgE) with high affinity, produce anti-cancer mediators such as tumor necrosis factor alpha (TNF-α) and granulocyte macrophage colony-stimulating factor (GM-CSF), and generally populate the tumor microenvironments. Yet, the role of MCs in cancer pathologies remains controversial with evidence for both anti-tumor and pro-tumor effects. Here, we review the studies examining the role of MCs in multiple forms of cancer, provide an alternative, MC-based hypothesis underlying the mechanism of therapeutic tumor IgE efficacy in clinical trials, and propose a novel strategy for using tumor-targeted, IgE-sensitized MCs as a platform for developing new cellular cancer immunotherapies. This autologous MC cancer immunotherapy could have several advantages over current cell-based cancer immunotherapies and provide new mechanistic strategies for cancer therapeutics alone or in combination with current approaches.

Gastric cancer (GC) is a malignancy with a high incidence and mortality. The tumor immune microenvironment plays an important role in promoting cancer development and supports GC progression. Accumulating evidence shows that GC cells can exert versatile mechanisms to remodel the tumor immune microenvironment and induce immune evasion. In this review, we systematically summarize the intricate crosstalk between GC cells and immune cells, including tumor-associated macrophages, neutrophils, myeloid-derived suppressor cells, natural killer cells, effector T cells, regulatory T cells, and B cells. We focus on how GC cells alter these immune cells to create an immunosuppressive microenvironment that protects GC cells from immune attack. We conclude by compiling the latest progression of immune checkpoint inhibitor-based immunotherapies, both alone and in combination with conventional therapies. Anti-cytotoxic T-lymphocyte-associated protein 4 and anti-programmed cell death protein 1/programmed death-ligand 1 therapy alone does not provide substantial clinical benefit for GC treatment. However, the combination of immune checkpoint inhibitors with chemotherapy or targeted therapy has promising survival advantages in refractory and advanced GC patients. This review provides a comprehensive understanding of the immune evasion mechanisms of GC, and highlights promising immunotherapeutic strategies.

• Gastric cancer
• Immune evasion
• Immune checkpoint
• Immunotherapy
• Microenvironment

• Cbl
• NK cells
• SHP-1
• immunotherapy
• nanoparticles

• Humans
• Immunotherapy
• Killer Cells, Natural
• Liposomes
• Nanoparticles
• Neoplasms/pathology
• Tumor Microenvironment

Chimeric antigen receptors (CARs) are fusion proteins with an extracellular antigen recognition domain and numerous intracellular signaling domains that have been genetically modified. CAR-engineered T lymphocyte-based therapies have shown great success against blood cancers; however, potential fatal toxicity, such as in cytokine release syndrome, and high costs are some shortcomings that limit the clinical application of CAR-engineered T lymphocytes and remain to overcome. Natural killer (NK) cells are the focal point of current immunological research owing to their receptors that prove to be promising immunotherapeutic candidates for treating cancer. However, to date, manipulation of NK cells to treat malignancies has been moderately successful. Recent progress in the biology of NK cell receptors has greatly transformed our understanding of how NK cells recognize and kill tumor and infected cells. CAR-NK cells may serve as an alternative candidate for retargeting cancer because of their unique recognition mechanisms, powerful cytotoxic effects especially on cancer cells in both CAR-dependent and CAR-independent manners and clinical safety. Moreover, NK cells can serve as an ‘off-the-shelf product’ because NK cells from allogeneic sources can also be used in immunotherapies owing to their reduced risk of alloreactivity. Although ongoing fundamental research is in the beginning stages, this review provides an overview of recent developments implemented to design CAR constructs to stimulate NK activation and manipulate NK receptors for improving the efficiency of immunotherapy against cancer, summarizes the preclinical and clinical advances of CAR-NK cells against both hematological malignancies and solid tumors and confronts current challenges and obstacles of their applications. In addition, this review provides insights into prospective novel approaches that further enhance the efficiency of CAR-NK therapies and highlights potential questions that require to be addressed in the future.

• CAR-NK
• CAR-T
• HLA
• KIR
• cancer immunotherapy
• clinical trials
• receptors
• tumor

Nowadays, new advances in society and health have brought an increased life expectancy. However, at the same time, aging comes with complications that impact the development of autoimmunity, neurodegenerative diseases and cancer. These complications affect the quality of life and impact the public health system. Specifically, with aging, a low-grade chronic sterile systemic inflammation with self-reactivity in the absence of acute infection occurs termed inflammaging. Inflammaging is related to an imbalanced immune response that can be either naturally acquired with aging or accelerated due to external triggers. Different molecules, metabolites and inflammatory forms of cell death are highly involved in these processes. Importantly, adoptive cellular immunotherapy is a modality of treatment for cancer patients that administers ex vivo expanded immune cells in the patient. The manipulation of these cells confers them enhanced proinflammatory properties. A general consequence of proinflammatory events is the development of autoimmune diseases and cancer. Herein, we review subsets of immune cells with a pertinent role in inflammaging, relevant proteins involved in these inflammatory events and external triggers that enhance and accelerate these processes. Moreover, we mention relevant preclinical studies that demonstrate associations of chronic inflammation with cancer development.

• NK cells
• SASP
• T cells
• immunosenescence
• immunotherapy
• inflammaging

Natural Killer (NK) cells are critical members of the innate immunity lymphocytes and have a critical role in host defense against malignant cells. Adoptive cell therapy (ACT) using chimeric antigen receptor (CAR) redirects the specificity of the immune cell against a target-specific antigen. ACT has recently created an outstanding opportunity for cancer treatment. Unlike CAR-armored T cells which hadnsome shortcomings as the CAR-receiving construct, Major histocompatibility complex (MHC)-independency, shorter lifespan, the potential to produce an off-the-shelf immune product, and potent anti-tumor properties of the NK cells has introduced NK cells as a potent alternative target for expression of CAR. Here, we aim to provide an updated overview on the current improvements in CAR NK design and immunobiology and describe the potential of CAR-modified NK cells as an alternative “off-the-shelf” carrier of CAR. We also provide lists for the sources of NK cells in the process of CAR NK cell production, different methods for transduction of the CAR genetic sequence to NK cells, the differences between CAR T and CAR NK, and CAR NK-targeted tumor antigens in current studies. Additionally, we provide data on recently published preclinical and clinical studies of CAR NK therapy and a list of finished and ongoing clinical trials. For achieving CAR NK products with higher efficacy and safety, we discuss current challenges in transduction and expansion of CAR NK cells, CAR NK therapy side effects, and challenges that limit the optimal efficacy of CAR NK cells and recommend possible solutions to enhance the persistence, function, safety, and efficacy of CAR NK cells with a special focus on solid tumors.

• Cancer
• Challenges
• Chimeric antigen receptor
• Immunotherapy
• Natural killer cell

Adoptive cellular immunotherapy using chimeric antigen receptor (CAR)-modified T cells and Natural Killer (NK) cells are common immune cell sources administered to treat cancer patients. In detail, whereas CAR-T cells induce outstanding responses in a subset of hematological malignancies, responses are much more deficient in solid tumors. Moreover, NK cells have not shown remarkable results up to date. In general, immune cells present high plasticity to change their activity and phenotype depending on the stimuli they receive from molecules secreted in the tumor microenvironment (TME). Consequently, immune cells will also secrete molecules that will shape the activities of other neighboring immune and tumor cells. Specifically, NK cells can polarize to activities as diverse as angiogenic ones instead of their killer activity. In addition, tumor cell phagocytosis by macrophages, which is required to remove dying tumor cells after the attack of NK cells or CAR-T cells, can be avoided in the TME. In addition, chemotherapy or radiotherapy treatments can induce senescence in tumor cells modifying their secretome to a known as “senescence-associated secretory phenotype” (SASP) that will also impact the immune response. Whereas the SASP initially attracts immune cells to eliminate senescent tumor cells, at high numbers of senescent cells, the SASP becomes detrimental, impacting negatively in the immune response. Last, CAR-T cells are an attractive option to overcome these events. Here, we review how molecules secreted in the TME by either tumor cells or even by immune cells impact the anti-tumor activity of surrounding immune cells.

• CAR-T cells
• NK cells
• SASP
• T cells
• immunotherapy
• macrophages
• senescence
• tumor secretome

• adaptive immunity
• chimeric antigen
• immunity
• immunotherapy
• innate
• killer cells
• natural
• receptors

• Chimeric antigen receptor (CAR)
• Hematological malignancies
• Immunotherapy
• Natural killer (NK) cells

• Hematologic Neoplasms/therapy
• Humans
• Immunotherapy, Adoptive
• Killer Cells, Natural
• Receptors, Chimeric Antigen/genetics
• T-Lymphocytes

• Cancer immunotherapy
• Chimeric antigen receptor
• Natural killer cells
• T cells

• Animals
• Genetic Engineering
• Humans
• Immunotherapy, Adoptive/methods
• Killer Cells, Natural/cytology
• Killer Cells, Natural/immunology
• Killer Cells, Natural/transplantation
• Neoplasms/immunology
• Neoplasms/therapy
• Receptors, Chimeric Antigen/genetics
• Receptors, Chimeric Antigen/therapeutic use
• Transduction, Genetic

• R01 AI129582 NIAID NIH HHS
• R01 NS106170 NINDS NIH HHS
• R21 CA223400 NCI NIH HHS
• R01 CA068458 NCI NIH HHS
• R35 CA210087 NCI NIH HHS
• P01 CA163205 NCI NIH HHS
• R01 CA247550 NCI NIH HHS
• National Institutes of Health

• NK cells
• cancer
• immunotherapy
• microbial infections

• CP042702 La Caixa Foundation
• PI17/01043 Instituto de Salud Carlos III

Cellular senescence was first described as a physiological tumor cell suppressor mechanism that leads to cell growth arrest with production of the senescence-associated secretory phenotype known as SASP. The main role of SASP in physiological conditions is to attract immune cells to clear senescent cells avoiding tumor development. However, senescence can be damage-associated and, depending on the nature of these stimuli, additional types of senescence have been described. In the context of cancer, damage-associated senescence has been described as a consequence of chemotherapy treatments that were initially thought of as a tumor suppressor mechanism. However, in certain contexts, senescence after chemotherapy can promote cancer progression, especially when immune cells become senescent and cannot clear senescent tumor cells. Moreover, aging itself leads to continuous inflammaging and immunosenescence which are responsible for rewiring immune cells to become defective in their functionality. Here, we define different types of senescence, pathways that activate them, and functions of SASP in these events. Additionally, we describe the role of senescence in cancer and its treatments, including how aging and chemotherapy contribute to senescence in tumor cells, before focusing on immune cell senescence and its role in cancer. Finally, we discuss potential therapeutic interventions to reverse cell senescence.

• SASP
• immunotherapy
• inflammaging
• senescence
• senescence surveillance

• Cellular Senescence
• Drug Resistance, Neoplasm/drug effects
• Drug Therapy
• Gene Regulatory Networks/drug effects
• Humans
• Immunotherapy/methods
• Neoplasms/drug therapy
• Neoplasms/immunology

• Immunotherapy
• Natural killer cells
• Ovarian cancer

• Cancer
• Immunotherapy
• NK cells
• Tumor microenvironment

• Animals
• Antigens, Neoplasm/immunology
• Antineoplastic Agents, Immunological/administration & dosage
• Combined Modality Therapy/methods
• Disease Models, Animal
• Drug Delivery Systems/methods
• Humans
• Immune Checkpoint Inhibitors/administration & dosage
• Immune Evasion/drug effects
• Immunologic Memory
• Immunotherapy/methods
• Killer Cells, Natural/drug effects
• Killer Cells, Natural/immunology
• Killer Cells, Natural/radiation effects
• Killer Cells, Natural/transplantation
• Magnetic Field Therapy
• Mice
• Nanomedicine/methods
• Nanoparticles/administration & dosage
• Neoplasms/immunology
• Neoplasms/therapy
• Oncolytic Viruses/immunology
• Receptors, Chimeric Antigen/immunology
• Tumor Microenvironment/drug effects
• Tumor Microenvironment/immunology
• Tumor Microenvironment/radiation effects

• NK cell
• arbovirus
• arthritis
• chikungunya
• granzyme A

Natural killer (NK) cells are important anti-tumor cells of our innate immune system. Their anti-cancer activity is mediated through interaction of a wide array of activating and inhibitory receptors with their ligands on tumor cells. After activation, NK cells also secrete a variety of pro-inflammatory molecules that contribute to the final immune response by modulating other innate and adaptive immune cells. In this regard, external proteins from NK cell secretome and the mechanisms by which they mediate these responses are poorly defined.

TRANS-stable-isotope labeling of amino acids in cell culture (TRANS-SILAC) combined with proteomic was undertaken to identify early materials transferred between cord blood-derived NK cells (CB-NK) and multiple myeloma (MM) cells. Further in vitro and in vivo studies with knock-down of histones and CD138, overexpression of histones and addition of exogenous histones were undertaken to confirm TRANS-SILAC results and to determine functional roles of this material transferred.

We describe a novel mechanism by which histones are actively released by NK cells early after contact with MM cells. We show that extracellular histones bind to the heparan sulfate proteoglycan CD138 on the surface of MM cells to promote the creation of immune-tumor cell clusters bringing immune and MM cells into close proximity, and thus facilitating not only NK but also T lymphocyte anti-MM activity.

This study demonstrates a novel immunoregulatory role of NK cells against MM cells mediated by histones, and an additional role of NK cells modulating T lymphocytes activity that will open up new avenues to design future immunotherapy clinical strategies.

• Cell-cell communication
• Histones
• Immunotherapy
• Multiple myeloma
• NK cells

Our understanding on the mechanisms of graft versus tumor/leukemia (GvT/GvL) and graft versus host (GvH) effects has tremendously evolved within the past decades. During the search for a mechanism that augments GvT/GvL without increasing GvH effects, natural killer (NK) cells have clearly attracted attention. Current approaches of NK cell immunotherapy for hematological malignancies involve using methods for in vivo potentiation of NK cell proliferation and activity; adoptive transfer of NK cells from autologous and allogeneic sources [cord blood mononuclear cells, peripheral blood mononuclear cells, CD34⁺ stem cells] and NK cell lines; and genetic modification of NK cells. Several cytokines, including interleukin-2 and interleukin-15 take part in the development of NK cells and have been shown to boost NK cell effects both in vivo and ex vivo. Monoclonal antibodies directed towards certain targets, including stimulating CD16, blockade of NK cell receptors, and redirection of cytotoxicity to tumor cells via bi- or tri-specific engagers may promote NK cell function. Despite the relative disappointment with autologous NK cell infusions, the future holds promise in adoptive transfer of allogeneic NK cells and the development of novel cellular therapeutic strategies, such as chimeric antigen receptor-modified NK cell immunotherapy. In this review, we summarize the current status of NK cell-related mechanisms in the therapy of hematologic malignancies, and discuss the future perspectives on adoptive NK cell transfer and other novel cellular immunotherapeutic strategies.

• Hematological malignancies
• Immuno-therapy
• Natural killer cells

• Natural killer cell
• immunotherapy
• magnetic resonance imaging
• pancreatic cancer

• R01 CA209886 NCI NIH HHS

• Interferon-gamma
• Interleukin (IL)-15
• Interleukin (IL)-27
• Natural killer (NK) cells
• Natural killer cell receptor

• cd4⁺cd25⁺foxp3⁺ treg cells
• cytotoxicity
• nk cells
• nkg2d
• suppression

• Animals
• Cytotoxicity, Immunologic
• Forkhead Transcription Factors/immunology
• Humans
• Interleukin-2 Receptor alpha Subunit/immunology
• Killer Cells, Natural/immunology
• Lymphocyte Activation
• Mice
• NK Cell Lectin-Like Receptor Subfamily K/physiology
• T-Lymphocytes, Regulatory/immunology

The most common cause of death in patients with acute myeloid leukemia (AML) who receive allogeneic hematopoietic stem cell transplantation (allo-HSCT) is AML relapse. Therefore, additive therapies post allo-HSCT have significant potential to prevent relapse. Natural killer (NK)-cell-based immunotherapies can be incorporated into the therapeutic armamentarium for the eradication of AML cells post allo-HSCT. In recent studies, NK cell-based immunotherapies, the use of adoptive NK cells, NK cells in combination with cytokines, immune checkpoint inhibitors, bispecific and trispecific killer cell engagers, and chimeric antigen receptor-engineered NK cells have all shown antitumor activity in AML patients. In this review, we will discuss the current strategies with these NK cell-based immunotherapies as possible therapies to cure AML patients post allo-HSCT. Additionally, we will discuss various means of immune escape in order to further understand the mechanism of NK cell-based immunotherapies against AML.

• acute myeloid leukemia
• allogeneic hematopoietic stem cell transplantation
• bispecific and trispecific killer cell engagers
• chimeric antigen receptors
• immune checkpoint
• immunotherapy
• natural killer cell

• bioinspired materials
• biopreservation
• cryoprotectants
• immunotherapy
• natural killer cells

• R01 EB015776 NIBIB NIH HHS

• CAR T cells
• CCR
• Chimeric Receptors
• NK receptors
• TCR gene transfer
• Tumor Immunotherapy

Gastric cancer (GC) is one of the most common cancers, with a high incidence of cancer death. Despite various therapeutic approaches, the cures and prognosis of advanced GC remain poor. Natural killer (NK) cells, which are known as important lymphocytes in innate immunity, play vital roles in suppressing GC initiation, progression, and metastases. A wide range of clinical settings shows that increasing the number of NK cells or improving NK cell antitumor activity is promising in GC patients. NK cell adoptive therapy (especially expanded NK cells) is a safe and well-tolerated method, which can enhance NK cell cytotoxicity against GC. Meanwhile, cytokines, immunomodulatory drugs, immune checkpoint blockades, antibodies, vaccines, and gene therapy have been found to directly or indirectly activate NK cells to improve their killing activity toward GC. In this review, we summarize recent advancements in the relationship between NK cells and GC and point out all the innovative strategies that can enhance NK cells' function to inhibit the growth of GC.

• adoptive therapy
• checkpoint blockades
• gastric cancer
• immunity
• natural killer cells

Natural killer (NK) cells are innate immune cells that can be activated rapidly to target abnormal and virus-infected cells without prior sensitization. With significant advancements in cell biology technologies, many NK cell lines have been established. Among these cell lines, NK-92 cells are not only the most widely used but have also been approved for clinical applications. Additionally, chimeric antigen receptor-modified NK-92 cells (CAR-NK-92 cells) have shown strong antitumor effects. In this review, we summarize established human NK cell lines and their biological characteristics, and highlight the applications of NK-92 cells and CAR-NK-92 cells in tumor immunotherapy.

• NK-92
• chimeric antigen receptor
• immunotherapy
• natural killer cell line
• tumor