Relevant bibliographies by topics / T cells. Natural immunity

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'T cells. Natural immunity'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "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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Dissertations / Theses on the topic "T cells. Natural immunity"

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Sutiwisesak, Rujapak. "Natural Polymorphism of Mycobacterium tuberculosis and CD8 T Cell Immunity." eScholarship@UMMS, 2020. https://escholarship.umassmed.edu/gsbs_diss/1076.

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Coevolution between Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis, and the human host has been documented for thousands of years. Interestingly, while T cell immunity is crucial for host protection and survival, T cell antigens are the most conserved region of the Mtb genome. Hypothetically, Mtb adapts under immune pressure to exploit T cell responses for its benefit from inflammation and tissue destruction for ultimately transmission. EsxH, a gene encoding immunodominant TB10.4 protein, however, contains polymorphic regions corresponding to T cell epitopes. Here, I present two complementary analyses to examine how Mtb modulates TB10.4 for immune evasion. First, I use a naturally occurring esxH polymorphic clinical Mtb isolate, 667, to investigate how A10T amino acid exchange in TB10.4 affect T cell immunity. To verify and identify the cause of the immunological differences, I construct isogenic strains expressing EsxHA10T or EsxHWT. In combination with our recent finding that TB10.44-11-specific CD8 T cells do not recognize Mtb-infected macrophages, we hypothesize that TB10.4 is a decoy antigen as it distracts host immunity from inducing other potentially protective responses. I examine whether an elimination of TB10.44-11-specific CD8 T cell response leads to a better host protective immunity. The studies of in vivo infection and in vitro recognition in this dissertation aim to provide a better understanding of the counteraction between immune evasion and protective immunity.
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Rydyznski, Carolyn E. "Natural Killer Cell Regulation of Humoral Immunity." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1535377157934852.

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Borysiewicz, L. K. "Cell mediated immunity to human cytomegalovirus infection (cytotoxic T cell and natural killer cell mediated lysis of human cytomegalovirus infected cells)." Thesis, Imperial College London, 1986. http://hdl.handle.net/10044/1/37949.

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Zhou, Jianfang. "The immunological roles of human macrophages in avian influenza virus infection." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36611153.

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Zhou, Jianfang, and 周劍芳. "The immunological roles of human macrophages in avian influenza virus infection." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B36611153.

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Mukherjee, Sumanta. "LPS induced T[subscript]H2 (Interleukin-4) cytokine production in macrophages and its regulation." Connect to full text in OhioLINK ETD Center, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1207743729.

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Dissertation (Ph.D.)--University of Toledo, 2008.
"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 161-180.
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Mayes, Kimberly. "The Role of the Nucleosome Remodeling Factor NURF in Inhibiting T and Natural Killer Cell Mediated Antitumor Immunity by Suppressing Tumor Antigenicity and Natural Cytotoxicity Receptor Co-ligands." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4770.

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Tumor immunoediting is a dynamic process in which the immune response attacks tumor cells by detecting danger signals and tumor antigens. In order to survive, tumor cells develop mechanisms to avoid detection or destruction by the immune system. To counteract this, several strategies are being developed to enhance the antitumor immune response, including the depletion of immunosuppressive cells, enhancing the activation of antitumor immune cells and increasing tumor cell immunogenicity. These therapies have seen limited success individually, however, and it is likely that combination therapy with novel targets will be necessary to see reproducible beneficial responses. Epigenetic modifications are attractive therapeutic targets because they are reversible and affect gene expression in cancer cells. Within this framework, this study aimed to elucidate the role of the chromatin remodeling complex nucleosome remodeling factor (NURF) in cancer immunoediting by silencing of bromodomain PHD-finger containing transcription factor (BPTF), the largest and essential subunit of NURF. Using two syngeneic mouse models of cancer, BPTF was found to suppress T cell antitumor activity in the tumor microenvironment. In vitro, enhanced cytolytic activity was observed for individual CD8 T cell clones only from mice bearing BPTF-silenced tumors, implicating the involvement of novel antigens. Mechanistic investigations revealed that NURF directly suppresses the expression of genes encoding immunoproteasome subunits Psmb8 and Psmb9 and the antigen transporter genes Tap1 and Tap2. PSMB8 inhibition reversed the effects of BPTF ablation, consistent with a critical role for the immunoproteasome in improving tumor immunogenicity. Thus, NURF normally suppresses tumor cell antigenicity and its depletion improves CD8 T cell antitumor immunity. In a concurrent study using different tumor lines, BPTF was also found to suppress natural killer (NK) cell antitumor immunity in vivo. Enhanced NK cell cytolytic activity toward BPTF-depleted targets in vitro was dependent on the natural cytotoxicity receptors (NCR). Molecular studies revealed that BPTF directly activates heparanase (Hpse) expression, resulting in reduced cell surface abundance of the NCR co-ligands: heparan sulfate proteoglycans. Thus, NURF represses NCR co-ligand abundance and its depletion enhances NK cell cytotoxicity. Therefore, NURF emerges as a candidate therapeutic target to enhance CD8 T or NK cell antitumor immunity.
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Watkin, Levi B. "The Role of Heterologous Immunity in Mediating Natural Resistance to Infection in Human Subjects: A Dissertation." eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/586.

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Heterologous immunity is a mechanism by which immunological memory within an individual, developed in response to a previous infection, plays a role in the immune response to a subsequent unrelated infection. In murine studies, heterologous immunity facilitated by cross-reactive CD8 T-cell responses can mediate either beneficial (protective immunity) or detrimental effects (e.g. enhanced lung and adipose immunopathology and enhanced viral titers) (Selin et al., 1998; Chen et al., 2001; Welsh and Selin, 2002; Nie et al., 2010; Welsh et al., 2010). Protective heterologous immunity results in enhanced clearance of virus during a subsequent infection with an unrelated pathogen. Such is the case when mice are immunized with lymphocytic choriomeningitis virus (LCMV) and subsequently challenged with Pichinde virus (PV) or vaccinia virus (VACV) (Selin et al., 1998). However, heterologous immunity may also mediate enhanced immunopathology as mice immunized with influenza A virus (IAV) and challenged with LCMV show increased viral titers and enhanced lung immunopathology (Chen et al., 2003). The role heterologous immunity plays during infection is not limited to the murine system. In fact, there have now been several reports of enhanced immunopathology due to heterologous immunity during human infections, involving viruses such as IAV, Epstein-Barr Virus (EBV), hepatitis C virus (HCV), and dengue virus (DENV) (Mathew et al., 1998; Wedemeyer et al., 2001; Acierno et al., 2003; Nilges et al., 2003; Clute et al., 2005; Urbani et al., 2005). Interestingly, in all reported cases in humans, heterologous immunity mediated enhanced immunopathology. Upon infection with EBV the clinical presentation can range from asymptomatic to severe, occasionally fatal, acute infectious mononucleosis (AIM) (Crawford et al., 2006b; Luzuriaga and Sullivan, 2010) which is marked by a massive CD8 lymphocytosis. This lympho-proliferative effect in AIM was shown to be partially mediated by reactivation of cross-reactive IAV-M1 58-66 (IAV-GIL) specific CD8 memory T-cells in HLA-A2 patients reacting to the EBV-BMLF1 280 (EBV-GLC) epitope (Clute et al., 2005). Interestingly, EBV infects ~90% of individuals globally by the third decade of life, establishing a life-long infection (Henle et al., 1969). However, it is unknown why 5-10% of adults remain EBV-sero-negative (EBV-SN), despite the fact that the virus infects the vast majority of the population and is actively shed at high titers even during chronic infection (Hadinoto et al., 2009). Here, we show that EBV-SN HLA-A2+ adults possess cross-reactive IAV-GIL/EBV-GLC memory CD8 T-cells that show highly unique properties. These IAV-GIL cross-reactive memory CD8 T-cells preferentially expand and produce cytokines to EBV antigens at high functional avidity. Additionally, they are capable of lysing EBV-infected targets and show the potential to enter the mucosal epithelial tissue, where infection is thought to initiate, by CD103 expression. This protective capacity of these cross-reactive memory CD8 T-cells may be explained by a unique T-cell receptor (TCR) repertoire that differs by both organization and CDR3 usage from that in EBV-seropositive (EBV-SP) donors. The composition of the CD8 T-cell repertoire is a dynamic process that begins during the stochastic positive selection of the T-cell pool during development in the thymus. Thus, upon egress to the periphery a naïve T-cell pool, or repertoire, is formed that is variable even between genetically identical individuals. This T-cell repertoire is not static, as each new infection leaves its mark on the repertoire once again by stochastically selecting and expanding best-fit effectors and memory populations to battle each new infection while at the same time deleting older memory CD8 T-cells to make room for the new memory cells (Selin et al., 1999). These events induce an altered repertoire that is unique to each individual at each infection. It is this dynamic and variable organization of the T-cell repertoire that leads to private specificity even between genetically identical individuals upon infection with the same pathogens and thus a different fate (Kim et al., 2005; Cornberg et al., 2006a; Nie et al., 2010). It is this private specificity of the TCR repertoire that helps explain why individuals with the same epitope specific cross-reactive response, but composed of different cross-reactive T-cell clones, can either develop AIM or never become infected with EBV. Our results suggest that heterologous immunity may protect EBV-SN adults against the establishment of productive EBV infection, and potentially be the first demonstration of protective T-cell heterologous immunity between unrelated pathogens in humans. Our results also suggest that CD8 T-cell immunity can be sterilizing and that an individual’s TCR repertoire ultimately determines their fate during infection. To conclusively show that heterologous immunity is actively protecting EBV-SN adults from the establishment of a productive EBV infection, one would have to deliberately expose an individual to the virus. Clearly, this is not an acceptable risk, and it could endanger the health of an individual. A humanized mouse model could allow one to address this question. However, before we can even attempt to address the question of heterologous immunity mediating protection from EBV infection in humanized mice, we must first determine whether these mice can be infected with, and build an immune response to the two viruses we are studying, EBV and IAV. We show here that these mice can indeed be infected with and also mount an immune response to EBV. Additionally, these mice can also be infected with IAV. However, at this time the immune responses that are made to these viruses in our established humanized mouse model are not substantial enough to fully mimic a human immune response capable of testing our hypothesis of heterologous immunity mediating protection from EBV infection. Although the immune response in these mice to EBV and IAV infection is not suitable for the testing of our model the data are promising, as the humanized mouse model is constantly improving. Hopefully, with constant improvements being made there will be a model that will duplicate a human immune system in its entirety. This thesis will be divided into 5 major chapters. The first chapter will provide an introduction to both general T-cell biology and also to the role of heterologous immunity in viral infection. The second chapter will provide the details of the experimental procedures that were performed to test our hypothesis. The third chapter will describe the main scientific investigation of the role of heterologous immunity in providing natural resistance to infection in human subjects. This chapter will also consist of the data that will be compiled into a manuscript for publication in a peer-reviewed journal. The fourth chapter will consist of work performed pertaining to the establishment of a humanized mouse model of EBV and IAV infection. The establishment of this model is important for us to be able to show causation for protection from EBV infection mediated by heterologous immunity.
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Wang, Lili. "The role of T cell immunity in natural influenza A infection in a UK cohort : flu watch." Thesis, University of Oxford, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.669930.

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A novel influenza A virus bearing the characteristics of high virulence, the ability to infect humans and transmit from human to human, such as the pandemic influenza of 1918, could lead to millions of deaths. The 2009 influenza pandemic demonstrated that a novel influenza A virus could spread globally in a few months despite the availability of modern comprehensive surveillance systems and systemic prevention and control measurements. Novel pandemic strains that could occur naturally or be created in laboratory, pose a serious threat to public health. Current available vaccines are capable to induce neutralizing antibodies against the viral surface antigen hemagglutinin (HA), which provide sterilizing immunity by blocking infection. However this antibody protection is serotype specific and therefore offers limited or no protection against a serologically distinct influenza virus. An alternative vaccine approach is the induction of cross-protective T cell immunity, directed at influenza A conserved internal proteins which could potentially offer broad protection against different influenza strains in humans. This approach may complement antibody-inducing vaccines and greatly enhance the protective efficacy of influenza vaccines. This study builds on previous evidence derived from animal models and human experimental challenge studies, to demonstrate the heterotypic T cell immunity in the context of natural influenza A infection in humans. Pre-existing influenza A specific T cell immunity was quantified by human IFN-γ ELISpot assay and was detectable in over 70% of Flu Watch participants. Nucleoprotein was the most immunodominant viral protein; and the most potent viral protein in eliciting influenza A specific CD8+ T cells. The nucleoprotein specific T cells exhibited high level of cross reactivity to the 2009 pandemic influenza and reduced the occurrence of nasal viral shedding in the absence of antibody immunity, following acquisition of pandemic influenza infections. This study provides evidence to support the development of a T cell based influenza vaccine, and provides important evidence to empower future studies of this kind.
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Batista, Mariana Dias. "Avaliação de aspectos inatos e adaptativos do sistema imune na psoríase: análise fenotípica e funcional de células natural killer e células T." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5146/tde-13032013-170151/.

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INTRODUÇÃO: A psoríase é doença inflamatória hiperproliferativa da pele, na qual mecanismos imunológicos são cruciais para o processo patogênico. O marcador CD57 denota inabilidade de replicação e imuno-senescência de células T CD8+, e sua expressão foi demonstrada em diversas condições inflamatórias. CD57 também pode ser expresso por células natural killer (NK), nas quais é considerado marcador de maturidade, por ser em geral adquirido pelas formas mais diferenciadas CD56+CD16+. A expressão de CD57 e outros receptores de células NK não foi amplamente investigada na psoríase. OBJETIVOS: Este estudo buscou examinar o fenótipo de células NK em biópsias de pele e células mononucleares do sangue periférico (CMSP) de pacientes com psoríase em relação a controles sadios. Este estudo investigou também o fenótipo e características funcionais de células T isoladas da pele lesional e não afetada de pacientes com psoríase. MÉTODOS: Foram isoladas células NK dos subtipos CD56+CD16- e CD56+CD16+ de pele lesional, não afetada e CMSP de pacientes com psoríase, comparadas com pele normal e CMSP de controles sadios. A expressão de CD57, NKG2A e NKG2C foi determinada nesses subtipos de células por citometria de fluxo. Células T CD4+ e CD8+ foram isoladas da pele lesional e não afetada de pacientes com psoríase, e a expressão de CD57 foi avaliada. Características funcionais de células T foram estudadas através da análise da secreção de diversas citocinas inflamatórias (IL-17A, IFN-\", IL-2, IL-33, TNF- #, IL-21, IL-22 and IL-27) produzidas por células T CD4+ e CD8+ isoladas por sorting celular, a partir de amostras de pele lesional e não afetada de pacientes com psoríase. RESULTADOS: Células NK isoladas das lesões de psoríase apresentaram um fenótipo particular, caracterizado por baixa expressão de CD57 e alta expressão de NKG2A na pele lesional e não afetada em relação aos controles. Em relação às células T, encontrouse frequência de células T CD4+CD57+ e CD8+CD57+ significativamente maior na pele não afetada em relação à pele lesional de pacientes com psoríase. Células T CD4+ isoladas por sorting celular a partir de amostras de pele lesional produziram níveis maiores de IL-17A, IL-22 e IFN-\" em relação às amostras de pele não afetada. Células T CD8+ isoladas da pele lesional secretaram maiores níveis de IL-17A, IFN-\", TNF-# e IL- 2 em relação à pele não afetada. CONCLUSÕES: Esses dados sugerem que células NK presentes nas lesões de psoríase apresentam fenótipo imaturo, que foi previamente associado a maiores capacidades funcionais, e poderiam ser implicadas na patogênese da psoríase. Em relação às células T, as características fenotípicas sugerem menor sobrevivência de células com baixa capacidade replicativa na pele lesional, pelo ambiente inflamatório local ou pelo alto turnover celular da psoríase
INTRODUCTION: Psoriasis is a hyper-proliferative inflammatory disease of the skin in which immunological mechanisms play a direct role in disease pathogenesis. CD57 is a marker of replicative inability and immunosenescence on CD8+ T cells and its expression is increased in a number of inflammatory conditions. CD57 is also expressed by NK cells and is considered a marker of NK cell maturity, being acquired by more differentiated CD56+CD16+ NK cells. The expression of CD57 and other NK cell markers in psoriasis has not been thoroughly investigated. OBJECTIVES: This study sought to examine the phenotype of NK cells in skin biopsies and peripheral blood mononuclear cells (PBMC) from patients with psoriasis and healthy controls. We also investigated the phenotype and functional characteristics of T cells from psoriasis patients, comparing lesional and unaffected skin. METHODS: CD56+CD16- and CD56+CD16+ NK cells were isolated from lesional skin, unaffected skin and PBMC of psoriasis patients, and normal skin and PBMC from healthy controls. The expression of CD57, NKG2A, and NKG2C was assessed by flow cytometry. CD57 expression was also determined on T cells from lesional and unaffected skin by flow cytometry. We assessed functional characteristics of T cells by evaluating the secretion of several inflammatory cytokines (IL-17A, IFN-\", IL- 2, IL-33, TNF-#, IL-21, IL-22 and IL-27), from cell-sorted purified CD4+ and CD8+ T cells isolated from lesional and unaffected skin of psoriasis patients, by multiplex assays. RESULTS: NK cells in psoriasis skin lesions exhibited a distinct phenotype, with CD57 expression significantly reduced and NKG2A expression increased on NK cells in lesional and unaffected skin compared to controls. In relation to T cells, we observed that the frequency of CD57+CD4+ and CD57+CD8+ T cells was significantly increased in unaffected skin of psoriasis patients compared to lesional skin. Sorted CD4+ T cells from psoriasis lesional skin produced higher levels of IL-17A, IL-22 and IFN-\" compared to unaffected skin. CD8+ T cells isolated from lesional skin produced higher levels of IL- 17A, IFN-\", TNF-# and IL-2 compared to unaffected skin. CONCLUSIONS: These data suggest that NK cells in psoriasis lesions exhibit an immature phenotype, that has been previously associated with higher functional abilities, and could implicate NK cells in psoriasis pathogenesis. For T cells, the findings of this study suggest lower survival of cells with low replicative ability in lesional skin, due to the local inflammatory environment or to the high cellular turnover in psoriasis
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Books on the topic "T cells. Natural immunity"

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A, Berzofsky Jay, and SpringerLink (Online service), eds. Natural Killer T cells: Balancing the Regulation of Tumor Immunity. New York, NY: Springer Science+Business Media, LLC, 2012.

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Guide to signal pathways in immune cells. New York: Springer Verlag, 2009.

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Wardle, E. N. Guide to signal pathways in immune cells. New York: Springer Verlag, 2009.

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Terabe, Masaki, and Jay A. Berzofsky, eds. Natural Killer T cells. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-0613-6.

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Memory T cells. New York: Springer Science+Business Media, 2010.

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Zanetti, M. Memory T cells. New York: Springer Science+Business Media, 2010.

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Liu, Chaohong, ed. Invariant Natural Killer T-Cells. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1775-5.

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W, Ades Edwin, and Lopez Carlos 1942-, eds. Natural killer cells and host defense. Basel: Karger, 1989.

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Lane, I. William. Immune power. Garden City Park, NY: Avery Pub. Group, 1999.

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1951-, Schmidt Reinhold E., ed. Natural Killer cells: Biology and clinical application. Basel: Karger, 1990.

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Book chapters on the topic "T cells. Natural immunity"

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O’Konek, Jessica J., Jay A. Berzofsky, and Masaki Terabe. "Immune Regulation of Tumor Immunity by NKT Cells." In Natural Killer T cells, 55–70. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0613-6_4.

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Kinjo, Yuki, and Mitchell Kronenberg. "DETECTION OF MICROBES BY NATURAL KILLER T CELLS." In Crossroads between Innate and Adaptive Immunity II, 17–26. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-79311-5_3.

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Arora, Pooja, Erin L. Foster, and Steven A. Porcelli. "CD1d and Natural Killer T Cells in Immunity to Mycobacterium tuberculosis." In Advances in Experimental Medicine and Biology, 199–223. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6111-1_11.

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Lambert, Eleonora E., Anne-Marie Buisman, and Cécile A. C. M. van Els. "Superior B. pertussis Specific CD4+ T-Cell Immunity Imprinted by Natural Infection." In Advances in Experimental Medicine and Biology, 81–98. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/5584_2019_405.

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Jiang, Jiansheng, Kannan Natarajan, and David H. Margulies. "MHC Molecules, T cell Receptors, Natural Killer Cell Receptors, and Viral Immunoevasins—Key Elements of Adaptive and Innate Immunity." In Advances in Experimental Medicine and Biology, 21–62. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-9367-9_2.

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André, Pascale, and Nicolas Anfossi. "Clinical Analysis of Human Natural Killer Cells." In Innate Immunity, 291–300. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-570-1_17.

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Bancroft, A. J., and R. K. Grencis. "Th1 and Th2 Cells and Immunity to Intestinal Helminths." In Mucosal T Cells, 192–208. Basel: KARGER, 1998. http://dx.doi.org/10.1159/000058711.

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Zanetti, Maurizio, Paola Castiglioni, and Elizabeth Ingulli. "Principles of Memory CD8 T-Cells Generation in Relation to Protective Immunity." In Memory T Cells, 108–25. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6451-9_9.

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Pezoldt, Joern, Juhao Yang, Mangge Zou, and Jochen Huehn. "Microbiome and Gut Immunity: T Cells." In The Gut Microbiome in Health and Disease, 119–40. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90545-7_9.

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Celli, Susanna, Béatrice Breart, and Philippe Bousso. "Intravital Two-Photon Imaging of Natural Killer Cells and Dendritic Cells in Lymph Nodes." In Innate Immunity, 119–26. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-570-1_7.

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Conference papers on the topic "T cells. Natural immunity"

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Kato, Shingo, Tetsuya Matsuura, Yoshitaka Hippo, and Atsushi Nakajima. "Abstract 4625: Natural killer T cells regulate tumor immunity in mouse pancreatic cancer organoid orthotropic model." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4625.

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Tode, Naoki, Toshiaki Kikuchi, Taizou Shibahara, Hisayoshi Daito, Arif Santoso, Tsutomu Tamada, Shinya Ohkouchi, Masahito Ebina, and Toshihiro Nukiwa. "Innate Immunity Mediated By Natural Killer T Cells Is Required For The Development Of Hot Tub Lung In Mice." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4247.

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Pilones, KA, and S. Demaria. "P1-01-05: Conditioning by the Tumor Environment Turns Invariant Natural Killer T Cells into Negative Regulators of Anti-Tumor Immunity Elicited by Treatment." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p1-01-05.

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Mulaosmanovic, H., C. Monzio Compagnoni, N. Castellani, G. Carnevale, D. Ventrice, P. Fantini, A. S. Spinelli, A. L. Lacaita, and A. Benvenuti. "Data regeneration and disturb immunity of T-RAM cells." In ESSDERC 2014 - 44th European Solid State Device Research Conference. IEEE, 2014. http://dx.doi.org/10.1109/essderc.2014.6948754.

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Rathmell, Jeffrey C. "Abstract SY33-02: Fueling T cells and antitumor immunity." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-sy33-02.

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Zhao, Ende, Tomasz Maj, Ilona Kryczek, Lili Zhao, Shuang Wei, Shanshan Wan, Joel Crespo, et al. "Abstract 4078: EZH2 marks polyfunctional memory T cells and controls tumor immunity." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4078.

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Pecher, A. C., F. Kettemann, J. Henes, S. Duerr-Stoerzer, C. Schneidawind, L. Kanz, and D. Schneidawind. "FRI0408 Invariant natural killer t cells in systemic sclerosis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.4531.

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Hao, Xingxing, Louis D. Falo, Guo Chen, Cara D. Carey, Louis D. Falo, and Zhaoyang You. "Abstract A37: Blockading PD1 on tumor-primed CD4 T cells instigates antitumor immunity." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a37.

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Baba, Junko, Satoshi Watanabe, Kosuke Ichikawa, Jun Koshio, Takao Miyabayashi, Junta Tanaka, Hiroshi Tanaka, Hiroshi Kagamu, Hirohisa Yoshizawa, and Ichiei Narita. "Abstract 1920: Chemo-resistant regulatory T cells inhibit the augmentation of antitumor immunity during homeostatic T cell proliferation." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1920.

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Su, Shicheng, Jianyou Liao, Jiang Liu, Qiang Liu, and Erwei Song. "Abstract 3959: CCL18-recruited naïve CD4+T cells are converted to tumor-infiltrating regulatory T cells in breast cancer and suppress antitumor immunity." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3959.

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Reports on the topic "T cells. Natural immunity"

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Paget, Christophe, Helene Duret, and Mark J. Smyth. Role of Natural Killer T Cells In Immunogenic Chemotherapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada571626.

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Chen, Xiuxu, and Jenny E. Gumperz. Human CD1d-Restricted Natural Killer T (NKT) Cell Cytotoxicity Against Myeloid Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada462826.

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Paget, Christophe, Helene Duret, and Mark J. Smyth. Role of Natural Killer T Cells in Immunogenic Chemotherapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada595285.

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