Journal articles: 'T cells. Natural immunity'

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Leadbetter, Elizabeth A., and Mikael C. I. Karlsson. "Invariant natural killer T cells balance B cell immunity." Immunological Reviews 299, no. 1 (January 2021): 93–107. http://dx.doi.org/10.1111/imr.12938.

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Lowdell, M. W. "Natural Killer T cells – balancing the regulation of tumor immunity." British Journal of Cancer 107, no. 10 (November 2012): 1795–96. http://dx.doi.org/10.1038/bjc.2012.453.

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Mercer, Jason C., Melanie J. Ragin, and Avery August. "Natural killer T cells: rapid responders controlling immunity and disease." International Journal of Biochemistry & Cell Biology 37, no. 7 (July 2005): 1337–43. http://dx.doi.org/10.1016/j.biocel.2004.11.019.

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Van Kaer, Luc, Vrajesh V. Parekh, and Lan Wu. "Invariant natural killer T cells: bridging innate and adaptive immunity." Cell and Tissue Research 343, no. 1 (August 24, 2010): 43–55. http://dx.doi.org/10.1007/s00441-010-1023-3.

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Kadowaki, Norimitsu, Svetlana Antonenko, Johnson Yiu-Nam Lau, and Yong-Jun Liu. "Natural Interferon α/β–Producing Cells Link Innate and Adaptive Immunity." Journal of Experimental Medicine 192, no. 2 (July 10, 2000): 219–26. http://dx.doi.org/10.1084/jem.192.2.219.

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Innate immune responses to pathogens critically impact the development of adaptive immune responses. However, it is not completely understood how innate immunity controls the initiation of adaptive immunities or how it determines which type of adaptive immunity will be induced to eliminate a given pathogen. Here we show that viral stimulation not only triggers natural interferon (IFN)-α/β–producing cells (IPCs) to produce vast amounts of antiviral IFN-α/β but also induces these cells to differentiate into dendritic cells (DCs). IFN-α/β and tumor necrosis factor α produced by virus-activated IPCs act as autocrine survival and DC differentiation factors, respectively. The virus-induced DCs stimulate naive CD4+ T cells to produce IFN-γ and interleukin (IL)-10, in contrast to IL-3–induced DCs, which stimulate naive CD4+ T cells to produce T helper type 2 cytokines IL-4, IL-5, and IL-10. Thus, IPCs may play two master roles in antiviral immune responses: directly inhibiting viral replication by producing large amounts of IFN-α/β, and subsequently triggering adaptive T cell–mediated immunity by differentiating into DCs. IPCs constitute a critical link between innate and adaptive immunity.

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Brutkiewicz, Randy R., and Venkataraman Sriram. "Natural killer T (NKT) cells and their role in antitumor immunity." Critical Reviews in Oncology/Hematology 41, no. 3 (March 2002): 287–98. http://dx.doi.org/10.1016/s1040-8428(01)00198-6.

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Paget, C., and F. Trottein. "Role of type 1 natural killer T cells in pulmonary immunity." Mucosal Immunology 6, no. 6 (October 9, 2013): 1054–67. http://dx.doi.org/10.1038/mi.2013.59.

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Kinjo, Yuki, Naoki Kitano, and Mitchell Kronenberg. "The role of invariant natural killer T cells in microbial immunity." Journal of Infection and Chemotherapy 19, no. 4 (2013): 560–70. http://dx.doi.org/10.1007/s10156-013-0638-1.

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Wu, Zeguang, Giada Frascaroli, Carina Bayer, Tatjana Schmal, and Thomas Mertens. "Interleukin-2 from Adaptive T Cells Enhances Natural Killer Cell Activity against Human Cytomegalovirus-Infected Macrophages." Journal of Virology 89, no. 12 (April 8, 2015): 6435–41. http://dx.doi.org/10.1128/jvi.00435-15.

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ABSTRACTControl of human cytomegalovirus (HCMV) requires a continuous immune surveillance, thus HCMV is the most important viral pathogen in severely immunocompromised individuals. Both innate and adaptive immunity contribute to the control of HCMV. Here, we report that peripheral blood natural killer cells (PBNKs) from HCMV-seropositive donors showed an enhanced activity toward HCMV-infected autologous macrophages. However, this enhanced response was abolished when purified NK cells were applied as effectors. We demonstrate that this enhanced PBNK activity was dependent on the interleukin-2 (IL-2) secretion of CD4+T cells when reexposed to the virus. Purified T cells enhanced the activity of purified NK cells in response to HCMV-infected macrophages. This effect could be suppressed by IL-2 blocking. Our findings not only extend the knowledge on the immune surveillance in HCMV—namely, that NK cell-mediated innate immunity can be enhanced by a preexisting T cell antiviral immunity—but also indicate a potential clinical implication for patients at risk for severe HCMV manifestations due to immunosuppressive drugs, which mainly suppress IL-2 production and T cell responsiveness.IMPORTANCEHuman cytomegalovirus (HCMV) is never cleared by the host after primary infection but instead establishes a lifelong latent infection with possible reactivations when the host′s immunity becomes suppressed. Both innate immunity and adaptive immunity are important for the control of viral infections. Natural killer (NK) cells are main innate effectors providing a rapid response to virus-infected cells. Virus-specific T cells are the main adaptive effectors that are critical for the control of the latent infection and limitation of reinfection. In this study, we found that IL-2 secreted by adaptive CD4+T cells after reexposure to HCMV enhances the activity of NK cells in response to HCMV-infected target cells. This is the first direct evidence that the adaptive T cells can help NK cells to act against HCMV infection.

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Welsh, Raymond M., Chin H. Tay, Steven M. Varga, Carey L. O'Donnell, Kristin L. Vergilis, and Liisa K. Selin. "Lymphocyte-dependent ‘natural’ immunity to virus infections mediated by both natural killer cells and memory T cells." Seminars in Virology 7, no. 2 (April 1996): 95–102. http://dx.doi.org/10.1006/smvy.1996.0012.

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Kanto, Tatsuya, and Norio Hayashi. "Innate immunity in hepatitis C virus infection: Interplay among dendritic cells, natural killer cells and natural killer T cells." Hepatology Research 37, s3 (October 2007): S319—S326. http://dx.doi.org/10.1111/j.1872-034x.2007.00236.x.

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Fujii, Shin-Ichiro, Kanako Shimizu, Hiroaki Hemmi, and Ralph M. Steinman. "Innate Vα14+natural killer T cells mature dendritic cells, leading to strong adaptive immunity." Immunological Reviews 220, no. 1 (December 2007): 183–98. http://dx.doi.org/10.1111/j.1600-065x.2007.00561.x.

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Altman, Jennie B., Adriana D. Benavides, Rupali Das, and Hamid Bassiri. "Antitumor Responses of Invariant Natural Killer T Cells." Journal of Immunology Research 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/652875.

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Natural killer T (NKT) cells are innate-like lymphocytes that were first described in the late 1980s. Since their initial description, numerous studies have collectively shed light on their development and effector function. These studies have highlighted the unique requirements for the activation of these lymphocytes and the functional responses that distinguish these cells from other effector lymphocyte populations such as conventional T cells and NK cells. This body of literature suggests that NKT cells play diverse nonredundant roles in a number of disease processes, including the initiation and propagation of airway hyperreactivity, protection against a variety of pathogens, development of autoimmunity, and mediation of allograft responses. In this review, however, we focus on the role of a specific lineage of NKT cells in antitumor immunity. Specifically, we describe the development of invariant NKT (iNKT) cells and the factors that are critical for their acquisition of effector function. Next, we delineate the mechanisms by which iNKT cells influence and modulate the activity of other immune cells to directly or indirectly affect tumor growth. Finally, we review the successes and failures of clinical trials employing iNKT cell-based immunotherapies and explore the future prospects for the use of such strategies.

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Ingram, Zewde, Shriya Madan, Jenoy Merchant, Zakiya Carter, Zen Gordon, Gregory Carey, and Tonya J. Webb. "Targeting Natural Killer T Cells in Solid Malignancies." Cells 10, no. 6 (May 27, 2021): 1329. http://dx.doi.org/10.3390/cells10061329.

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Natural killer T (NKT) cells are a unique subset of lymphocytes that recognize lipid antigens in the context of the non-classical class I MHC molecule, CD1d, and serve as a link between the innate and adaptive immune system through their expeditious release of cytokines. Whereas NKT have well-established roles in mitigating a number of human diseases, herein, we focus on their role in cancer. NKT cells have been shown to directly and indirectly mediate anti-tumor immunity and manipulating their effector functions can have therapeutic significances in treatment of cancer. In this review, we highlight several therapeutic strategies that have been used to harness the effector functions of NKT cells to target different types of solid tumors. We also discuss several barriers to the successful utilization of NKT cells and summarize effective strategies being developed to harness the unique strengths of this potent population of T cells. Collectively, studies investigating the therapeutic potential of NKT cells serve not only to advance our understanding of this powerful immune cell subset, but also pave the way for future treatments focused on the modulation of NKT cell responses to enhance cancer immunotherapy.

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Raphael, Itay, Rachel R. Joern, and Thomas G. Forsthuber. "Memory CD4+ T Cells in Immunity and Autoimmune Diseases." Cells 9, no. 3 (February 25, 2020): 531. http://dx.doi.org/10.3390/cells9030531.

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CD4+ T helper (Th) cells play central roles in immunity in health and disease. While much is known about the effector function of Th cells in combating pathogens and promoting autoimmune diseases, the roles and biology of memory CD4+ Th cells are complex and less well understood. In human autoimmune diseases such as multiple sclerosis (MS), there is a critical need to better understand the function and biology of memory T cells. In this review article we summarize current concepts in the field of CD4+ T cell memory, including natural history, developmental pathways, subsets, and functions. Furthermore, we discuss advancements in the field of the newly-described CD4+ tissue-resident memory T cells and of CD4+ memory T cells in autoimmune diseases, two major areas of important unresolved questions in need of answering to advance new vaccine design and development of novel treatments for CD4+ T cell-mediated autoimmune diseases.

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Seidel, Andreas, Corinna L. Seidel, Matthias Weider, Rüdiger Junker, Lina Gölz, and Helga Schmetzer. "Influence of Natural Killer Cells and Natural Killer T Cells on Periodontal Disease: A Systematic Review of the Current Literature." International Journal of Molecular Sciences 21, no. 24 (December 21, 2020): 9766. http://dx.doi.org/10.3390/ijms21249766.

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Natural killer (NK) cells, as members of the innate immune system, and natural killer T (NKT) cells, bridging innate and adaptive immunity, play a prominent role in chronic inflammatory diseases and cancerogenesis, yet have scarcely been examined in oral diseases. Therefore, systematic research on the latest literature focusing on NK/NKT cell-mediated mechanisms in periodontal disease, including the time period 1988–2020, was carried out in MEDLINE (PubMed) using a predetermined search strategy, with a final selection of 25 studies. The results showed that NK cells tend to have rather proinflammatory influences via cytokine production, cytotoxic effects, dendritic-cell-crosstalk, and autoimmune reactions, while contrarily, NKT cell-mediated mechanisms were proinflammatory and immunoregulatory, ranging from protective effects via B-cell-regulation, specific antibody production, and the suppression of autoimmunity to destructive effects via cytokine production, dendritic-cell-crosstalk, and T-/B-cell interactions. Since NK cells seem to have a proinflammatory role in periodontitis, further research should focus on the proinflammatory and immunoregulatory properties of NKT cells in order to create, in addition to antibacterial strategies in dental inflammatory disease, novel anti-inflammatory therapeutic approaches modulating host immunity towards dental health.

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Wang, Y., S. Sedimbi, L. Löfbom, A. K. Singh, S. A. Porcelli, and S. L. Cardell. "Unique invariant natural killer T cells promote intestinal polyps by suppressing TH1 immunity and promoting regulatory T cells." Mucosal Immunology 11, no. 1 (April 12, 2017): 131–43. http://dx.doi.org/10.1038/mi.2017.34.

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Gonzalez-Aseguinolaza, Gloria, Luc Van Kaer, Cornelia C. Bergmann, James M. Wilson, John Schmieg, Mitchell Kronenberg, Toshinori Nakayama, Masaru Taniguchi, Yasuhiko Koezuka, and Moriya Tsuji. "Natural Killer T Cell Ligand α-Galactosylceramide Enhances Protective Immunity Induced by Malaria Vaccines." Journal of Experimental Medicine 195, no. 5 (March 4, 2002): 617–24. http://dx.doi.org/10.1084/jem.20011889.

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The important role played by CD8+ T lymphocytes in the control of parasitic and viral infections, as well as tumor development, has raised the need for the development of adjuvants capable of enhancing cell-mediated immunity. It is well established that protective immunity against liver stages of malaria parasites is primarily mediated by CD8+ T cells in mice. Activation of natural killer T (NKT) cells by the glycolipid ligand, α-galactosylceramide (α-GalCer), causes bystander activation of NK, B, CD4+, and CD8+ T cells. Our study shows that coadministration of α-GalCer with suboptimal doses of irradiated sporozoites or recombinant viruses expressing a malaria antigen greatly enhances the level of protective anti-malaria immunity in mice. We also show that coadministration of α-GalCer with various different immunogens strongly enhances antigen-specific CD8+ T cell responses, and to a lesser degree, Th1-type responses. The adjuvant effects of α-GalCer require CD1d molecules, Vα14 NKT cells, and interferon γ. As α-GalCer stimulates both human and murine NKT cells, these findings should contribute to the design of more effective vaccines against malaria and other intracellular pathogens, as well as tumors.

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Münz, Christian, Ralph M. Steinman, and Shin-ichiro Fujii. "Dendritic cell maturation by innate lymphocytes." Journal of Experimental Medicine 202, no. 2 (July 18, 2005): 203–7. http://dx.doi.org/10.1084/jem.20050810.

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Pathogen recognition by Toll-like receptors (TLRs) on dendritic cells (DCs) leads to DC maturation and the initiation of adaptive immunity. Recent studies have shown that innate lymphocytes—natural killer (NK), natural killer T (NKT), and γδ T cells—also trigger DC maturation. This interaction in turn expands and activates innate lymphocytes and initiates adaptive T cell immunity. Here, we comment on the evidence that these pathways are TLR independent and have the potential to respond to infection, malignancy, and immunotherapy.

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Ehlers, Margret, Claudia Papewalis, Wiebke Stenzel, Benedikt Jacobs, Klaus L. Meyer, René Deenen, Holger S. Willenberg, et al. "Immunoregulatory Natural Killer Cells Suppress Autoimmunity by Down-Regulating Antigen-Specific CD8+ T Cells in Mice." Endocrinology 153, no. 9 (September 1, 2012): 4367–79. http://dx.doi.org/10.1210/en.2012-1247.

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Natural killer (NK) cells belong to the innate immune system. Besides their role in antitumor immunity, NK cells also regulate the activity of other cells of the immune system, including dendritic cells, macrophages, and T cells, and may, therefore, be involved in autoimmune processes. The aim of the present study was to clarify the role of NK cells within this context. Using two mouse models for type 1 diabetes mellitus, a new subset of NK cells with regulatory function was identified. These cells were generated from conventional NK cells by incubation with IL-18 and are characterized by the expression of the surface markers CD117 (also known as c-Kit, stem cell factor receptor) and programmed death (PD)-ligand 1. In vitro analyses demonstrated a direct lysis activity of IL-18-stimulated NK cells against activated insulin-specific CD8+ T cells in a PD-1/PD-ligand 1-dependent manner. Flow cytometry analyses revealed a large increase of splenic and lymphatic NK1.1+/c-Kit+ NK cells in nonobese diabetic mice at 8 wk of age, the time point of acceleration of adaptive cytotoxic immunity. Adoptive transfer of unstimulated and IL-18-stimulated NK cells into streptozotocin-treated mice led to a delayed diabetes development and partial disease prevention in the group treated with IL-18-stimulated NK cells. Consistent with these data, mild diabetes was associated with increased numbers of NK1.1+/c-Kit+ NK cells within the islets. Our results demonstrate a direct link between innate and adaptive immunity in autoimmunity with newly identified immunoregulatory NK cells displaying a potential role as immunosuppressors.

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Miyahira, Yasushi, Masaharu Katae, Kazuyoshi Takeda, Hideo Yagita, Ko Okumura, Seiki Kobayashi, Tsutomu Takeuchi, Tsuneo Kamiyama, Yoshinosuke Fukuchi, and Takashi Aoki. "Activation of Natural Killer T Cells by α-Galactosylceramide Impairs DNA Vaccine-Induced Protective Immunity against Trypanosoma cruzi." Infection and Immunity 71, no. 3 (March 2003): 1234–41. http://dx.doi.org/10.1128/iai.71.3.1234-1241.2003.

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ABSTRACT Innate immunity as a first defense is indispensable for host survival against infectious agents. We examined the roles of natural killer (NK) T cells in defense against Trypanosoma cruzi infection. The T. cruzi parasitemia and survival of CD1d-deficient mice exhibited no differences compared to wild-type littermates. NK T-cell activation induced by administering α-galactosylceramide (α-GalCer) to T. cruzi-infected mice significantly changed the parasitemia only in the late phase of infection and slightly improved survival when mice were infected intraperitoneally. The combined usage of α-GalCer and benznidazole, a commercially available drug for Chagas' disease, did not enhance the therapeutic efficacy of benznidazole. These results suggest that NK T cells do not play a pivotal role in resistance to T. cruzi infection. In addition, we found that the coadministration of α-GalCer with DNA vaccine impaired the induction of epitope-specific CD8+ T cells and undermined the DNA vaccine-induced protective immunity against T. cruzi. Our results, in contrast to previous reports demonstrating the protective roles of NK T cells against other infectious agents, suggest that these cells might even exhibit adverse effects on vaccine-mediated protective immunity.

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Ruggeri, Loredana, Emanuela Burchielli, Katia Perruccio, Marusca Capanni, Martin Stern, Kathrin Hafen, Franco Aversa, et al. "Alloreactive Natural Killer Cells Rebuild Adaptive Immunity to Infections after Haploidentical Hematopoietic Transplantation." Blood 108, no. 11 (November 16, 2006): 3210. http://dx.doi.org/10.1182/blood.v108.11.3210.3210.

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Abstract Transplantation of peripheral blood hematopoietic cells from HLA haplotype-mismatched family members is a therapeutic strategy for patients with high-risk acute leukemia who need transplantation and do not have matched donors. As T cell alloreactions cause lethal GvHD in mismatched transplants, only T cell-depleted hematopoietic grafts can be used. In adults, because of declining thymic function, immune-recovery originates from expansion of the mature T cells infused with the graft. In T cell depleted mismatched transplant immune recovery is hindered by the paucity of the starting T-cell population. Slow recovery of functional T cell immunity to pathogens is responsible for 35% infection-related mortality which remains the most pressing clinical issue. In murine MHC-haploidentical bone marrow transplant models we demonstrated donor-versus-recipient alloreactive NK cells ablate recipient-type lympho-hematopietic cells such as leukemic cells, the T cells that cause rejection and the antigen-presenting cells which trigger GvHD. Consequently mismatched T cell-replete transplants can be performed without GvHD (Ruggeri et al., Science 2002). Unexpectedly, in recent experiments, we observed alloreactive NK cells hastened immune-reconstitution. Pre-transplant infusion of alloreactive NK cells promoted brisk recovery of donor B and T cell precursors which matured correctly and of donor DCs. Rapidly reconstistuting DCs were crcuicial in protecting mice from infectious challenges. We next demonstrated:interaction between alloreactive NK cells and NK-susceptible recipient DCs alone was responsible for immune-rebuilding,NK conditioned mice remain receptive to accelerated immune rebuilding even when transplanted a week after NK conditioning, therefore the NK-DC interaction appears to release an as yet unknown immune-rebuilding factor which acts upon bone marrow and thymus microenvironements stably over time,quantitative PCR on bone marrow and thimus of NK conditioned mice shows several-fold increased expression of cytokines implicated in B, T and myeloid cell maturation, such as IL-7 and c-Kit ligand;the accelerated immune rebuilding effect can be reproduced by conditioning mice with the infusion of NK:DC co-culture supernatants. These observation prompted an analysis of infectious mortality in 178 acute leukemia patients who received haploidentical transplant at our Center. Transplantation from KIR ligand-mismatched (i.e., NK alloreactive) donors, in addition to controlling AML relapse, offers statistically significant protection from infectious mortality in AML and ALL patients. Studies are in progress to identify “immune rebuilding factor(s)”, produced in consequence of the interaction between donor alloreactive NK and recipient DCs, in the hope they might be exploited to boost immune-recovery and help reduce infection mortality after haploidentical hematopoietic transplantation.

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Jonsdottir, I. H., A. Asea, P. Hoffmann, U. I. Dahlgren, B. Andersson, K. Hellstrand, and P. Thoren. "Voluntary chronic exercise augments in vivo natural immunity in rats." Journal of Applied Physiology 80, no. 5 (May 1, 1996): 1799–803. http://dx.doi.org/10.1152/jappl.1996.80.5.1799.

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The effect of chronic voluntary exercise on the immune response was studied in spontaneously hypertensive rats. Exercise consisted of voluntary running in wheels for 5 wk, and the mean running distance was 4.2 km/24 h. In vivo cytotoxicity was measured as clearance of injected 51Cr-labeled YAC-1 lymphoma cells from the lungs. The clearance of YAC-1 cells in vivo was significantly increased in runners compared with sedentary controls (P < 0.001). The total number of mononuclear cells in the spleen was significantly decreased in runners compared with controls. Analysis of splenic lymphocyte phenotypes revealed a significantly increased fraction of OX52+/CD5- natural killer cells in runners compared with sedentary controls. In contrast to changes in natural immunity, immunoglobulins G and M levels in serum, the antibody response to antigen in vivo, and the proliferation of splenic T cells in vitro were unchanged. Our data suggest that chronic voluntary exercise augments natural cytotoxicity mechanisms in vivo, whereas splenic T-cell proliferation and the antibody-mediated immune response remain unchanged.

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Joyee, Antony George, Hongyu Qiu, Yijun Fan, Shuhe Wang, and Xi Yang. "Natural Killer T Cells Are Critical for Dendritic Cells to Induce Immunity in Chlamydial Pneumonia." American Journal of Respiratory and Critical Care Medicine 178, no. 7 (October 2008): 745–56. http://dx.doi.org/10.1164/rccm.200804-517oc.

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Guan, Jun, Gang Wang, Qin Yang, Chao Chen, Jingwen Deng, Xinyu Gu, and Haihong Zhu. "Natural Killer T Cells in Various Mouse Models of Hepatitis." BioMed Research International 2021 (January 6, 2021): 1–9. http://dx.doi.org/10.1155/2021/1782765.

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Natural killer T (NKT) cells are a key component of innate immunity. Importantly, a growing body of evidence indicates that NKT cells play an integral role in various acute and chronic liver injuries. NKT cells participate in the progression of an injury through the secretion of cytokines, which promote neutrophil infiltration and enhance Fas ligand (FasL) and granzyme-mediated NKT cytotoxic activity. Therefore, examining the role of NKT cells in hepatic disease is critical for a comprehensive understanding of disease pathogenesis and may provide insight into novel approaches for treatment. For more than a century, mouse models that imitate the physiopathological conditions of human disease have served as a critical tool in biological and medical basic research, including studies of liver disease. Here, we review the role of NKT cells in various mouse models of hepatitis.

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Ocaña-Morgner, Carlos, Maria M. Mota, and Ana Rodriguez. "Malaria Blood Stage Suppression of Liver Stage Immunity by Dendritic Cells." Journal of Experimental Medicine 197, no. 2 (January 20, 2003): 143–51. http://dx.doi.org/10.1084/jem.20021072.

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Malaria starts with Plasmodium sporozoites infection of the host's liver, where development into blood stage parasites occurs. It is not clear why natural infections do not induce protection against the initial liver stage and generate low CD8+ T cell responses. Using a rodent malaria model, we show that Plasmodium blood stage infection suppresses CD8+ T cell immune responses that were induced against the initial liver stage. Blood stage Plasmodium affects dendritic cell (DC) functions, inhibiting maturation and the capacity to initiate immune responses and inverting the interleukin (IL)-12/IL-10 secretion pattern. The interaction of blood stage parasites with DCs induces the secretion of soluble factors that inhibit the activation of CD8+ T cells in vitro and the suppression of protective CD8+ T cell responses against the liver stage in vivo. We propose that blood stage infection induces DCs to suppress CD8+ T cell responses in natural malaria infections. This evasion mechanism leaves the host unprotected against reinfection by inhibiting the immune response against the initial liver stage of the disease.

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Warncke, Max, Maike Buchner, Gudrun Thaller, Anna Dodero, Alla Bulashevska, Dietmar Pfeifer, Jens Timmer, and Hendrik Veelken. "Control of the specificity of T cell-mediated anti-idiotype immunity by natural regulatory T cells." Cancer Immunology, Immunotherapy 60, no. 1 (September 17, 2010): 49–60. http://dx.doi.org/10.1007/s00262-010-0918-x.

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O'Leary, Jacqueline G., Mahmoud Goodarzi, Danielle L. Drayton, and Ulrich H. von Andrian. "T cell– and B cell–independent adaptive immunity mediated by natural killer cells." Nature Immunology 7, no. 5 (April 16, 2006): 507–16. http://dx.doi.org/10.1038/ni1332.

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de Aguiar, Cristhiane Favero, Angela Castoldi, Mariane T. Amano, Aline Ignacio, Fernanda Fernandes Terra, Mario Cruz, Raphael J. F. Felizardo, et al. "Fecal IgA Levels and Gut Microbiota Composition Are Regulated by Invariant Natural Killer T Cells." Inflammatory Bowel Diseases 26, no. 5 (December 10, 2019): 697–708. http://dx.doi.org/10.1093/ibd/izz300.

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Abstract Background The gut microbiota is a key element to support host homeostasis and the development of the immune system. The relationship between the microbiota and immunity is a 2-way road, in which the microbiota contributes to the development/function of immune cells and immunity can affect the composition of microbes. In this context, natural killer T cells (NKT cells) are distinct T lymphocytes that play a role in gut immunity and are influenced by gut microbes. In our work, we investigated the involvement of invariant NKT cells (iNKT) in intestinal homeostasis. Results We found that iNKT-deficient mice (iNKT-KO) had reduced levels of fecal IgA and an altered composition of the gut microbiota, with increased Bacteroidetes. The absence of iNKT cells also affected TGF-β1 levels and plasma cells, which were significantly reduced in knockout (KO) mice. In addition, when submitted to dextran sodium sulfate colitis, iNKT-KO mice had worsening of colitis when compared with wild-type (WT) mice. To further address iNKT cell contribution to intestinal homeostasis, we adoptively transferred iNKT cells to KO mice, and they were submitted to colitis. Transfer of iNKT cells improved colitis and restored fecal IgA levels and gut microbiota. Conclusions Our results indicate that intestinal NKT cells are important modulators of intestinal homeostasis and that gut microbiota composition may be a potential target in the management of inflammatory bowel diseases.

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Correia, Margareta P., Ana Stojanovic, Katharina Bauer, Dilafruz Juraeva, Lars-Oliver Tykocinski, Hanns-Martin Lorenz, Benedikt Brors, and Adelheid Cerwenka. "Distinct human circulating NKp30+FcεRIγ+CD8+T cell population exhibiting high natural killer-like antitumor potential." Proceedings of the National Academy of Sciences 115, no. 26 (June 12, 2018): E5980—E5989. http://dx.doi.org/10.1073/pnas.1720564115.

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CD8+T cells are considered prototypical cells of adaptive immunity. Here, we uncovered a distinct CD8+T cell population expressing the activating natural killer (NK) receptor NKp30 in the peripheral blood of healthy individuals. We revealed that IL-15 could de novo induce NKp30 expression in a population of CD8+T cells and drive their differentiation toward a broad innate transcriptional landscape. The adaptor FcεRIγ was concomitantly induced and was shown to be crucial to enable NKp30 cell-surface expression and function in CD8+T cells. FcεRIγ de novo expression required promoter demethylation and was accompanied by acquisition of the signaling molecule Syk and the “innate” transcription factor PLZF. IL-15–induced NKp30+CD8+T cells exhibited high NK-like antitumor activity in vitro and were able to synergize with T cell receptor signaling. Importantly, this population potently controlled tumor growth in a preclinical xenograft mouse model. Our study, while blurring the borders between innate and adaptive immunity, reveals a unique NKp30+FcεRIγ+CD8+T cell population with high antitumor therapeutic potential.

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Burger, Eva. "Paracoccidioidomycosis Protective Immunity." Journal of Fungi 7, no. 2 (February 13, 2021): 137. http://dx.doi.org/10.3390/jof7020137.

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Protective immunity against Paracoccidioides consists of a stepwise activation of numerous effector mechanisms that comprise many cellular and soluble components. At the initial phase of non-specific innate immunity, resistance against Paracoccidioides comes from phagocytic polymorphonuclear neutrophils, natural killer (NK) cells and monocytes, supplemented by soluble factors such as cytokines and complement system components. Invariant receptors (Toll-like receptors (TLRs), Dectins) which are present in cells of the immune system, detect patterns present in Paracoccidioides (but not in the host) informing the hosts cells that there is an infection in progress, and that the acquired immunity must be activated. The role of components involved in the innate immunity of paracoccidioidomycosis is herein presented. Humoral immunity, represented by specific antibodies which control the fungi in the blood and body fluids, and its role in paracoccidioidomycosis (which was previously considered controversial) is also discussed. The protective mechanisms (involving various components) of cellular immunity are also discussed, covering topics such as: lysis by activated macrophages and cytotoxic T lymphocytes, the participation of lytic products, and the role of cytokines secreted by T helper lymphocytes in increasing the efficiency of Paracoccidioides, lysis.

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Kitajima, Masayuki, Toshihiro Ito, Damon J. Tumes, Yusuke Endo, Atsushi Onodera, Kahoko Hashimoto, Shinichiro Motohashi, et al. "Memory Type 2 Helper T Cells Induce Long-Lasting Antitumor Immunity by Activating Natural Killer Cells." Cancer Research 71, no. 14 (June 6, 2011): 4790–98. http://dx.doi.org/10.1158/0008-5472.can-10-1572.

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Choudhury, Hasib R., Nadeem A. Sheikh, Gregory J. Bancroft, David R. Katz, and J. Brian de Souza. "Early Nonspecific Immune Responses and Immunity to Blood-Stage Nonlethal Plasmodium yoelii Malaria." Infection and Immunity 68, no. 11 (November 1, 2000): 6127–32. http://dx.doi.org/10.1128/iai.68.11.6127-6132.2000.

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ABSTRACT The early role of natural killer cells and gamma delta T cells in the development of protective immunity to the blood stage of nonlethalPlasmodium yoelii infection was studied. Splenic cytokine levels were measured 24 h after infection of natural killer cell-depleted immunodeficient and littermate mice or transiently T-cell-depleted normal mice. Splenic gamma interferon levels were significantly increased above background in immunodeficient and littermate mice 24 h after infection. Depletion of natural killer cells resulted in markedly depressed gamma interferon levels and poor control of parasitemia, particularly in severe combined immunodeficient mice. In the littermates, gamma interferon levels were partially reduced, but parasitemias were resolved normally. However, in athymic mice, natural killer cell depletion had no effect on gamma interferon production. Levels of tumor necrosis factor alpha were increased in all animals 24 h after infection, and responses were not affected by natural killer cell depletion. However, in T-cell-depleted animals, both gamma interferon and tumor necrosis factor alpha levels were decreased 24 h after infection, and depleted mice were unable to control their parasitemia. These results suggest that the early production of both cytokines is important in the early control of parasitemia and that both natural killer and gamma delta T cells contribute equally towards their production. The data also suggest that the subsequent resolution of infection requires early production of gamma interferon, which might act by switching on the appropriate T-helper-cell subsets and other essential parasitotoxic effector mechanisms.

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Nikzad, Rana, Laura S. Angelo, Kevin Aviles-Padilla, Duy T. Le, Vipul K. Singh, Lynn Bimler, Milica Vukmanovic-Stejic, et al. "Human natural killer cells mediate adaptive immunity to viral antigens." Science Immunology 4, no. 35 (May 10, 2019): eaat8116. http://dx.doi.org/10.1126/sciimmunol.aat8116.

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Adaptive immune responses are defined as antigen sensitization–dependent and antigen-specific responses leading to establishment of long-lived immunological memory. Although natural killer (NK) cells have traditionally been considered cells of the innate immune system, mounting evidence in mice and nonhuman primates warrants reconsideration of the existing paradigm that B and T cells are the sole mediators of adaptive immunity. However, it is currently unknown whether human NK cells can exhibit adaptive immune responses. We therefore tested whether human NK cells mediate adaptive immunity to virally encoded antigens using humanized mice and human volunteers. We found that human NK cells displayed vaccination-dependent, antigen-specific recall responses in vitro, when isolated from livers of humanized mice previously vaccinated with HIV-encoded envelope protein. Furthermore, we discovered that large numbers of cytotoxic NK cells with a tissue-resident phenotype were recruited to sites of varicella-zoster virus (VZV) skin test antigen challenge in VZV-experienced human volunteers. These NK-mediated recall responses in humans occurred decades after initial VZV exposure, demonstrating that NK memory in humans is long-lived. Our data demonstrate that human NK cells exhibit adaptive immune responses upon vaccination or infection. The existence of human memory NK cells may allow for the development of vaccination-based approaches capable of establishing potent NK-mediated memory functions contributing to host protection.

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Leung, Briana, and Hobart W. Harris. "NKT Cells in Sepsis." Clinical and Developmental Immunology 2010 (2010): 1–10. http://dx.doi.org/10.1155/2010/414650.

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Sepsis is currently a leading cause of death in hospital intensive care units. Previous studies suggest that the pathophysiology of sepsis involves the hyperactivation of complex proinflammatory cascades that include the activation of various immune cells and the exuberant secretion of proinflammatory cytokines by these cells. Natural killer T-cells (NKTs) are a sublineage of T cells that share characteristics of conventional T cells and NK cells and bridge innate and adaptive immunity. More recently, NKT cells have been implicated in microbial immunity, including the onset of sepsis. Moreover, apolipoprotein E (apoE), a component of triglyceride-rich lipoproteins, has been shown to be protective in endotoxemia and gram-negative infections in addition to its well-known role in lipid metabolism. Here, we will review the role of NKT cells in sepsis and septic shock, the immunoregulatory role of apoE in the host immune response to infection, and propose a mechanism for this immunoregulation.

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Sato, Yuki, Eisaku Ogawa, and Ryuhei Okuyama. "Role of Innate Immune Cells in Psoriasis." International Journal of Molecular Sciences 21, no. 18 (September 9, 2020): 6604. http://dx.doi.org/10.3390/ijms21186604.

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Psoriasis is a chronic inflammatory skin condition caused by a combination of hereditary and environmental factors. Its development is closely related to the adaptive immune response. T helper 17 cells are major IL-17-producing cells, a function that plays an important role in the pathogenesis of psoriasis. However, recent findings have demonstrated that innate immune cells also contribute to the development of psoriasis. Innate lymphoid cells, γδ T cells, natural killer T cells, and natural killer cells are activated in psoriasis, contributing to disease pathology through IL-17-dependent and -independent mechanisms. The present review provides an overview of recent findings, demonstrating a role for innate immunity in psoriasis.

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Ebihara, Takashi. "Dichotomous Regulation of Acquired Immunity by Innate Lymphoid Cells." Cells 9, no. 5 (May 11, 2020): 1193. http://dx.doi.org/10.3390/cells9051193.

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The concept of innate lymphoid cells (ILCs) includes both conventional natural killer (NK) cells and helper ILCs, which resemble CD8+ killer T cells and CD4+ helper T cells in acquired immunity, respectively. Conventional NK cells are migratory cytotoxic cells that find tumor cells or cells infected with microbes. Helper ILCs are localized at peripheral tissue and are responsible for innate helper-cytokine production. Helper ILCs are classified into three subpopulations: TH1-like ILC1s, TH2-like ILC2s, and TH17/TH22-like ILC3s. Because of the functional similarities between ILCs and T cells, ILCs can serve as an innate component that augments each corresponding type of acquired immunity. However, the physiological functions of ILCs are more plastic and complicated than expected and are affected by environmental cues and types of inflammation. Here, we review recent advances in understanding the interaction between ILCs and acquired immunity, including T- and B-cell responses at various conditions. Immune suppressive activities by ILCs in particular are discussed in comparison to their immune stimulatory effects to gain precise knowledge of ILC biology and the physiological relevance of ILCs in human diseases.

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Renukaradhya, Gourapura J., Venkataraman Sriram, Wenjun Du, Jacquelyn Gervay-Hague, Luc Van Kaer, and Randy R. Brutkiewicz. "Inhibition of antitumor immunity by invariant natural killer T cells in a T-cell lymphoma modelin vivo." International Journal of Cancer 118, no. 12 (2006): 3045–53. http://dx.doi.org/10.1002/ijc.21764.

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Bedard, Melissa, Dilip Shrestha, David A. Priestman, Yuting Wang, Falk Schneider, Juan D. Matute, Shankar S. Iyer, et al. "Sterile activation of invariant natural killer T cells by ER-stressed antigen-presenting cells." Proceedings of the National Academy of Sciences 116, no. 47 (November 5, 2019): 23671–81. http://dx.doi.org/10.1073/pnas.1910097116.

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Invariant NKT (iNKT) cells have the unique ability to shape immunity during antitumor immune responses and other forms of sterile and nonsterile inflammation. Recent studies have highlighted a variety of classes of endogenous and pathogen-derived lipid antigens that can trigger iNKT cell activation under sterile and nonsterile conditions. However, the context and mechanisms that drive the presentation of self-lipid antigens in sterile inflammation remain unclear. Here we report that endoplasmic reticulum (ER)-stressed myeloid cells, via signaling events modulated by the protein kinase RNA-like ER kinase (PERK) pathway, increase CD1d-mediated presentation of immunogenic endogenous lipid species, which results in enhanced iNKT cell activation both in vitro and in vivo. In addition, we demonstrate that actin cytoskeletal reorganization during ER stress results in an altered distribution of CD1d on the cell surface, which contributes to enhanced iNKT cell activation. These results define a previously unidentified mechanism that controls iNKT cell activation during sterile inflammation.

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Lu, Liaoxun, Junjian Hu, Tianzhu Chao, Zhijun Chen, Zhuangzhuang Liu, Xinsong Luo, Yinming Liang, Pei He, and Lichen Zhang. "Loss of natural resistance to schistosome in T cell deficient rat." PLOS Neglected Tropical Diseases 14, no. 12 (December 21, 2020): e0008909. http://dx.doi.org/10.1371/journal.pntd.0008909.

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Schistosomiasis is among the major neglected tropical diseases and effective prevention by boosting the immune system is still not available. T cells are key cellular components governing adaptive immune response to various infections. While common laboratory mice, such as C57BL/6, are highly susceptible to schistosomiasis, the SD rats are extremely resistant. However, whether adaptive immunity is necessary for such natural resistance to schistosomiasis in rats remains to be determined. Therefore, it is necessary to establish genetic model deficient in T cells and adaptive immunity on the resistant SD background, and to characterize liver pathology during schistosomiasis. In this study we compared experimental schistosomiasis in highly susceptible C57BL/6 (B6) mice and in resistant SD rats, using cercariae of Schistosoma japonicum. We observed a marked T cell expansion in the spleen of infected B6 mice, but not resistant SD rats. Interestingly, CD3e−/− B6 mice in which T cells are completely absent, the infectious burden of adult worms was significantly higher than that in WT mice, suggesting an anti-parasitic role for T cells in B6 mice during schistosome infection. In further experiments, we established Lck deficient SD rats by using CRISPR/Cas9 in which T cell development was completely abolished. Strikingly, we found that such Lck deficiency in SD rats severely impaired their natural resistance to schistosome infection, and fostered parasite growth. Together with an additional genetic model deficient in T cells, the CD3e−/− SD rats, we confirmed the absence of T cell resulted in loss of natural resistance to schistosome infection, but also mitigated liver immunopathology. Our further experiments showed that regulatory T cell differentiation in infected SD rats was significantly decreased during schistosomiasis, in contrast to significant increase of regulatory T cells in infected B6 mice. These data suggest that T cell mediated immune tolerance facilitates persistent infection in mice but not in SD rats. The demonstration of an important role for T cells in natural resistance of SD rats to schistosomiasis provides experimental evidences supporting the rationale to boost T cell responses in humans to prevent and treat schistosomiasis.

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Suvas, Susmit, Uday Kumaraguru, Christopher D. Pack, Sujin Lee, and Barry T. Rouse. "CD4+CD25+ T Cells Regulate Virus-specific Primary and Memory CD8+ T Cell Responses." Journal of Experimental Medicine 198, no. 6 (September 15, 2003): 889–901. http://dx.doi.org/10.1084/jem.20030171.

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Naturally occurring CD4+CD25+ regulatory T cells appear important to prevent activation of autoreactive T cells. This article demonstrates that the magnitude of a CD8+ T cell–mediated immune response to an acute viral infection is also subject to control by CD4+CD25+ T regulatory cells (Treg). Accordingly, if natural Treg were depleted with specific anti-CD25 antibody before infection with HSV, the resultant CD8+ T cell response to the immunodominant peptide SSIEFARL was significantly enhanced. This was shown by several in vitro measures of CD8+ T cell reactivity and by assays that directly determine CD8+ T cell function, such as proliferation and cytotoxicity in vivo. The enhanced responsiveness in CD25-depleted animals was between three- and fourfold with the effect evident both in the acute and memory phases of the immune response. Surprisingly, HSV infection resulted in enhanced Treg function with such cells able to suppress CD8+ T cell responses to both viral and unrelated antigens. Our results are discussed both in term of how viral infection might temporarily diminish immunity to other infectious agents and their application to vaccines. Thus, controlling suppressor effects at the time of vaccination could result in more effective immunity.

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Ito, Hiroyasu, and Mitsuru Seishima. "Regulation of the Induction and Function of Cytotoxic T Lymphocytes by Natural Killer T Cell." Journal of Biomedicine and Biotechnology 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/641757.

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Cytotoxic T lymphocytes (CTLs) play a crucial role in the infections and the antitumor immunity. Induction and activation of antigen-specific CTLs is an important strategy in immunotherapy for various diseases, and several researchers have focused on the modulation of CTL induction and function. Natural killer T (NKT) cells are an important focus area of researchers studying immunomodulatory responses to tumors and infectious diseases. CD1d-restricted NKT cells consist of type I NKT cells and type II NKT cells. -galactosylceramide (-GalCer)-activated type I NKT cells secrete both Th1 (e.g., IFN-) and Th2 cytokines, affect the expression of costimulatory molecules in immune cells, and regulate the host immune system. Type II NKT cells, however, are stimulated by sulfatide, a self-glycolipid derived from myelin, and play an immunosuppressive role in animal model of autoimmune diseases. CTL generation, activation, and suppression are strongly affected by activated type I and type II NKT cells. Thus, the regulation of these NKT cells leads to the modification of CTL function. CTLs contribute to antimicrobial responses, antitumor immune and autoimmune responses. Understanding the role of NKT cells in the regulation of CTL generation, activation, and suppression enable the development of novel treatment strategies for these diseases.

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Barsac, Emilie, Carolina de Amat Herbozo, Loïc Gonzalez, Thomas Baranek, Thierry Mallevaey, and Christophe Paget. "Regulation and Functions of Protumoral Unconventional T Cells in Solid Tumors." Cancers 13, no. 14 (July 16, 2021): 3578. http://dx.doi.org/10.3390/cancers13143578.

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The vast majority of studies on T cell biology in tumor immunity have focused on peptide-reactive conventional T cells that are restricted to polymorphic major histocompatibility complex molecules. However, emerging evidence indicated that unconventional T cells, including γδ T cells, natural killer T (NKT) cells and mucosal-associated invariant T (MAIT) cells are also involved in tumor immunity. Unconventional T cells span the innate–adaptive continuum and possess the unique ability to rapidly react to nonpeptide antigens via their conserved T cell receptors (TCRs) and/or to activating cytokines to orchestrate many aspects of the immune response. Since unconventional T cell lineages comprise discrete functional subsets, they can mediate both anti- and protumoral activities. Here, we review the current understanding of the functions and regulatory mechanisms of protumoral unconventional T cell subsets in the tumor environment. We also discuss the therapeutic potential of these deleterious subsets in solid cancers and why further feasibility studies are warranted.

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Djaoud, Zakia, and Peter Parham. "HLAs, TCRs, and KIRs, a Triumvirate of Human Cell-Mediated Immunity." Annual Review of Biochemistry 89, no. 1 (June 20, 2020): 717–39. http://dx.doi.org/10.1146/annurev-biochem-011520-102754.

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In all human cells, human leukocyte antigen (HLA) class I glycoproteins assemble with a peptide and take it to the cell surface for surveillance by lymphocytes. These include natural killer (NK) cells and γδ T cells of innate immunity and αβ T cells of adaptive immunity. In healthy cells, the presented peptides derive from human proteins, to which lymphocytes are tolerant. In pathogen-infected cells, HLA class I expression is perturbed. Reduced HLA class I expression is detected by KIR and CD94:NKG2A receptors of NK cells. Almost any change in peptide presentation can be detected by αβ CD8+ T cells. In responding to extracellular pathogens, HLA class II glycoproteins, expressed by specialized antigen-presenting cells, present peptides to αβ CD4+ T cells. In comparison to the families of major histocompatibility complex (MHC) class I, MHC class II and αβ T cell receptors, the antigenic specificity of the γδ T cell receptors is incompletely understood.

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Shekhar, Sudhanshu, Antony George Joyee, and Xi Yang. "Invariant Natural Killer T Cells: Boon or Bane in Immunity to Intracellular Bacterial Infections?" Journal of Innate Immunity 6, no. 5 (2014): 575–84. http://dx.doi.org/10.1159/000361048.

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Chang, Wen-Chun, Chao-Hsu Li, Ling-Hui Chu, Pei-Shen Huang, Bor-Ching Sheu, and Su-Cheng Huang. "Regulatory T Cells Suppress Natural Killer Cell Immunity in Patients With Human Cervical Carcinoma." International Journal of Gynecological Cancer 26, no. 1 (January 2016): 156–62. http://dx.doi.org/10.1097/igc.0000000000000578.

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Morandi, Fabio, Mahboubeh Yazdanifar, Claudia Cocco, Alice Bertaina, and Irma Airoldi. "Engineering the Bridge between Innate and Adaptive Immunity for Cancer Immunotherapy: Focus on γδ T and NK Cells." Cells 9, no. 8 (July 22, 2020): 1757. http://dx.doi.org/10.3390/cells9081757.

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Most studies on genetic engineering technologies for cancer immunotherapy based on allogeneic donors have focused on adaptive immunity. However, the main limitation of such approaches is that they can lead to severe graft-versus-host disease (GvHD). An alternative approach would bolster innate immunity by relying on the natural tropism of some subsets of the innate immune system, such as γδ T and natural killer (NK) cells, for the tumor microenvironment and their ability to kill in a major histocompatibility complex (MHC)-independent manner. γδ T and NK cells have the unique ability to bridge innate and adaptive immunity while responding to a broad range of tumors. Considering these properties, γδ T and NK cells represent ideal sources for developing allogeneic cell therapies. Recently, significant efforts have been made to exploit the intrinsic anti-tumor capacity of these cells for treating hematologic and solid malignancies using genetic engineering approaches such as chimeric antigen receptor (CAR) and T cell receptor (TCR). Here, we review over 30 studies on these two approaches that use γδ T and NK cells in adoptive cell therapy (ACT) for treating cancer. Based on those studies, we propose several promising strategies to optimize the clinical translation of these approaches.

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Oberhardt, Valerie, Hendrik Luxenburger, Janine Kemming, Isabel Schulien, Kevin Ciminski, Sebastian Giese, Benedikt Csernalabics, et al. "Rapid and stable mobilization of CD8+ T cells by SARS-CoV-2 mRNA vaccine." Nature 597, no. 7875 (July 28, 2021): 268–73. http://dx.doi.org/10.1038/s41586-021-03841-4.

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AbstractSARS-CoV-2 spike mRNA vaccines1–3 mediate protection from severe disease as early as ten days after prime vaccination3, when neutralizing antibodies are hardly detectable4–6. Vaccine-induced CD8+ T cells may therefore be the main mediators of protection at this early stage7,8. The details of their induction, comparison to natural infection, and association with other arms of vaccine-induced immunity remain, however, incompletely understood. Here we show on a single-epitope level that a stable and fully functional CD8+ T cell response is vigorously mobilized one week after prime vaccination with bnt162b2, when circulating CD4+ T cells and neutralizing antibodies are still weakly detectable. Boost vaccination induced a robust expansion that generated highly differentiated effector CD8+ T cells; however, neither the functional capacity nor the memory precursor T cell pool was affected. Compared with natural infection, vaccine-induced early memory T cells exhibited similar functional capacities but a different subset distribution. Our results indicate that CD8+ T cells are important effector cells, are expanded in the early protection window after prime vaccination, precede maturation of other effector arms of vaccine-induced immunity and are stably maintained after boost vaccination.

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de Araújo, Nilberto Dias, Fábio Magalhães Gama, Mateus de Souza Barros, Thaís Lohana Pereira Ribeiro, Fabíola Silva Alves, Lilyane Amorim Xabregas, Andréa Monteiro Tarragô, Adriana Malheiro, and Allyson Guimarães Costa. "Translating Unconventional T Cells and Their Roles in Leukemia Antitumor Immunity." Journal of Immunology Research 2021 (January 7, 2021): 1–15. http://dx.doi.org/10.1155/2021/6633824.

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Recently, cell-mediated immune response in malignant neoplasms has become the focus in immunotherapy against cancer. However, in leukemia, most studies on the cytotoxic potential of T cells have concentrated only on T cells that recognize peptide antigens (Ag) presented by polymorphic molecules of the major histocompatibility complex (MHC). This ignores the great potential of unconventional T cell populations, which include gamma-delta T cells (γδ), natural killer T cells (NKT), and mucosal-associated invariant T cells (MAIT). Collectively, these T cell populations can recognize lipid antigens, specially modified peptides and small molecule metabolites, in addition to having several other advantages, which can provide more effective applications in cancer immunotherapy. In recent years, these cell populations have been associated with a repertoire of anti- or protumor responses and play important roles in the dynamics of solid tumors and hematological malignancies, thus, encouraging the development of new investigations in the area. This review focuses on the current knowledge regarding the role of unconventional T cell populations in the antitumor immune response in leukemia and discusses why further studies on the immunotherapeutic potential of these cells are needed.

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de Araújo, Nilberto Dias, Fábio Magalhães Gama, Mateus de Souza Barros, Thaís Lohana Pereira Ribeiro, Fabíola Silva Alves, Lilyane Amorim Xabregas, Andréa Monteiro Tarragô, Adriana Malheiro, and Allyson Guimarães Costa. "Translating Unconventional T Cells and Their Roles in Leukemia Antitumor Immunity." Journal of Immunology Research 2021 (January 7, 2021): 1–15. http://dx.doi.org/10.1155/2021/6633824.

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Recently, cell-mediated immune response in malignant neoplasms has become the focus in immunotherapy against cancer. However, in leukemia, most studies on the cytotoxic potential of T cells have concentrated only on T cells that recognize peptide antigens (Ag) presented by polymorphic molecules of the major histocompatibility complex (MHC). This ignores the great potential of unconventional T cell populations, which include gamma-delta T cells (γδ), natural killer T cells (NKT), and mucosal-associated invariant T cells (MAIT). Collectively, these T cell populations can recognize lipid antigens, specially modified peptides and small molecule metabolites, in addition to having several other advantages, which can provide more effective applications in cancer immunotherapy. In recent years, these cell populations have been associated with a repertoire of anti- or protumor responses and play important roles in the dynamics of solid tumors and hematological malignancies, thus, encouraging the development of new investigations in the area. This review focuses on the current knowledge regarding the role of unconventional T cell populations in the antitumor immune response in leukemia and discusses why further studies on the immunotherapeutic potential of these cells are needed.

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Journal articles on the topic 'T cells. Natural immunity'

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