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1.
Strong homeostatic TCR signals induce formation of self‐tolerant virtual memory CD8 T cells
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Daniel Mueller Martina Huranova Veronika Horkova Michaela Pribikova Robert Ivanek Susanne Oberle Dietmar Zehn Kathy D McCoy Peter Draber Ondrej Stepanek 《The EMBO journal》2018,37(14)
Virtual memory T cells are foreign antigen‐inexperienced T cells that have acquired memory‐like phenotype and constitute 10–20% of all peripheral CD8+ T cells in mice. Their origin, biological roles, and relationship to naïve and foreign antigen‐experienced memory T cells are incompletely understood. By analyzing T‐cell receptor repertoires and using retrogenic monoclonal T‐cell populations, we demonstrate that the virtual memory T‐cell formation is a so far unappreciated cell fate decision checkpoint. We describe two molecular mechanisms driving the formation of virtual memory T cells. First, virtual memory T cells originate exclusively from strongly self‐reactive T cells. Second, the stoichiometry of the CD8 interaction with Lck regulates the size of the virtual memory T‐cell compartment via modulating the self‐reactivity of individual T cells. Although virtual memory T cells descend from the highly self‐reactive clones and acquire a partial memory program, they are not more potent in inducing experimental autoimmune diabetes than naïve T cells. These data underline the importance of the variable level of self‐reactivity in polyclonal T cells for the generation of functional T‐cell diversity. 相似文献
2.
The p60 and NamA autolysins from Listeria monocytogenes contribute to host colonization and induction of protective memory
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Brian Weinrick Marilyn Gros Aurel Frangaj Massilva Rahmoun William R. Jacobs Jr Grégoire Lauvau 《Cellular microbiology》2015,17(2):147-163
Inducing long‐term protective memory CD8+ T‐cells is a desirable goal for vaccines against intracellular pathogens. However, the mechanisms of differentiation of CD8+ T‐cells into long‐lived memory cells capable of mediating protection of immunized hosts remain incompletely understood. We have developed an experimental system using mice immunized with wild type (WT) or mutants of the intracellular bacterium Listeria monocytogenes (Lm) that either do or do not develop protective memory CD8+ T‐cells. We previously reported that mice immunized with Lm lacking functional SecA2, an auxiliary secretion system of gram‐positive bacteria, did not differentiate functional memory CD8+ T‐cells that protected against a challenge infection with WT Lm. Herein we hypothesized that the p60 and NamA autolysins of Lm, which are major substrates of the SecA2 pathway, account for this phenotype. We generated Lm genetically deficient for genes encoding for the p60 and NamA proteins, ΔiapΔmurA Lm, and further characterized this mutant. Δp60ΔNamA Lm exhibited a strong filamentous phenotype, inefficiently colonized host tissues, and grew mostly outside cells. When Δp60ΔNamA Lm was made single unit, cell invasion was restored to WT levels during vaccination, yet induced memory T‐cells still did not protect immunized hosts against recall infection. Recruitment of blood phagocytes and antigen‐presenting cell activation was close to that of mice immunized with ΔActA Lm, which develop protective memory. However, key inflammatory factors involved in optimal T‐cell programming such as IL‐12 and type I IFN (IFN‐I) were lacking, suggesting that cytokine signals may largely account for the observed phenotype. Thus, altogether, these results establish that p60 and NamA secreted by Lm promote primary host cell invasion, the inflammatory response and the differentiation of functional memory CD8+ T‐cells, by preventing Lm filamentation during growth and subsequent triggering of innate sensing mechanisms. 相似文献
3.
Zhou L Li K Shi YL Hamzavi I Gao TW Henderson M Huggins RH Agbai O Mahmoud B Mi X Lim HW Mi QS 《Pigment cell & melanoma research》2012,25(5):602-611
Although it is widely believed that non‐segmental vitiligo (NSV) results from the autoimmune destruction of melanocytes, a clear understanding of defects in immune tolerance, which mediate this uncontrolled self‐reactivity, is still lacking. In the present study, we systemically evaluated circulating regulatory T (Treg) cells, including CD4+CD25+FoxP3+ Treg cells and invariant natural killer T (iNKT) cells, as well as naïve and memory CD4+ and CD8+ T cells and their cytokine production, in a cohort of 43 progressive NSV patients with race‐, gender‐, and age‐matched healthy controls. We found that the general immunophenotypes of CD4+ and CD8+ T cells and the percentage of CD4+CD25+FoxP3+ Tregs were comparable between NSV and healthy controls. However, percentages of peripheral iNKT cells were significantly decreased in NSV patients compared to that in healthy controls. Our data confirm the previous notion that the percentage of peripheral CD4+CD25+FoxP3+ Tregs remains unaltered in NSV and suggests the involvement of defective iNKT cells in the pathogenesis of NSV. 相似文献
4.
Helmin-Basa A Michalkiewicz J Gackowska L Kubiszewska I Eljaszewicz A Mierzwa G Bala G Czerwionka-Szaflarska M Prokurat A Marszalek A 《Helicobacter》2011,16(1):27-35
Background: In this study, H. pylori‐infected and noninfected children with gastritis were compared to a control group with respect to circulating CD4+ and CD8+ T lymphocytes expressing activation and differentiation markers. Additionally, the lymphocyte phenotypes of children with gastritis were correlated with the gastric inflammation scores. Materials and Methods: H. pylori infection status was assessed based on [13C]urea breath test, rapid urease test, and histology. Analysis of the lymphocyte surface molecule expression was carried out by triple‐color flow cytometry. Results: The group of H. pylori‐infected children showed an elevated proportion of peripheral B cells with CD19low, along with a twofold increase in the percentage of memory (CD45RO+) CD4+ and CD8+ T‐cell subsets (p < .05). Moreover, a positive correlation between the age and the percentage of these subsets was seen (r = .38, p = .04 and r = .56, p < .01, respectively). Children with gastritis but without infection had a slightly increased percentage of CD8+ T cells and CD56+ NK cells, CD3high T cells and CD45ROhigh CD4+ T‐cell subsets (p < .05). Both H. pylori‐infected and noninfected children with gastritis were characterized by an increased percentage of memory/effector CD4+ T cells, the presence of NK cells with CD56high, memory T‐cell subset with CD4high, and naive, memory, memory/effector, and effector T‐cell subsets with CD8high (p < .05). Gastric inflammation scores correlated positively with the percentage of CD4+ T lymphocytes in H. pylori‐infected children (r = .42, p = .03). In noninfected children, gastric inflammation scores correlated positively with the percentage of B cells (r = .45, p = .04). Conclusion: In H. pylori‐negative children, gastritis was associated with an increased percentage of activated NK and T cells, and intermediate‐differentiated peripheral blood CD4+ T cells, which was more pronounced in H. pylori‐positive children who also showed an increased B‐cell response. However, increased inflammation was only associated with the elevation of CD4+ T‐cell percentage in H. pylori‐positive children as well as B‐cell percentage in H. pylori‐negative children with gastritis. 相似文献
5.
Haruna Takeda Lino Tessarollo Neal G. Copeland Nancy A. Jenkins 《Genesis (New York, N.Y. : 2000)》2013,51(2):128-134
The RNA‐binding protein Musashi1 (Msi1) is one of two mammalian homologues of DrosophilaMusashi, which is required for the asymmetric cell division of sensory organ precursor cells. In the mouse central nervous system (CNS), Msi1 is preferentially expressed in mitotically active progenitor cells in the ventricular zone (VZ) of the neural tube during embryonic development and in the subventricular zone (SVZ) of the postnatal brain. Previous studies showed that cells in the SVZ can contribute to long‐term neurogenesis in the olfactory bulb (OB), but it remains unclear whether Msi1‐expressing cells have self‐renewing potential and can contribute to neurogenesis in the adult. Here, we describe the generation of Msi1‐CreERT2 knock‐in mice and show by cell lineage tracing that Msi1‐CreERT2‐expressing cells mark neural stem cells (NSCs) in both the embryonic and adult brain. Msi1‐CreERT2 mice thus represent a new tool in our arsenal for genetically manipulating NSCs, which will be essential for understanding the molecular mechanisms underlying neural development. genesis, 51:128–134, 2013. © 2012 Wiley Periodicals, Inc. 相似文献
6.
Transcriptional memory of cells of origin overrides β‐catenin requirement of MLL cancer stem cells
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Magdalena Zarowiecki Tsz Kan Fung Maria Mallardo Chiou‐Tsun Tsai Priscilla Nga Ieng Lau Quoc Chinh Hoang Pedro Veiga Jo Barnes Claire Lynn Amanda Wilson Boris Lenhard Chi Wai Eric So 《The EMBO journal》2017,36(21):3139-3155
7.
Jiangping Li Jun Zhao Juan Shen Changyou Wu Jie Liu 《Journal of cellular and molecular medicine》2019,23(1):596-609
Sustained adaptive immunity to pathogens provides effective protection against infections, and effector cells located at the site of infection ensure rapid response to the challenge. Both are essential for the success of vaccine development. To explore new vaccination approach against Mycobacterium tuberculosis (M.tb) infection, we have shown that Rv3615c, identified as ESX‐1 substrate protein C of M.tb but not expressed in BCG, induced a dominant Th1‐type response of CD4+ T cells from patients with tuberculosis pleurisy, which suggests a potential candidate for vaccine development. But subcutaneous immunization with Rv3615c induced modest T‐cell responses systemically, and showed suboptimal protection against virulent M.tb challenge at the site of infection. Here, we use a mouse model to demonstrate that intranasal immunization with Rv3615c induces sustained capability of adaptive CD4+ T‐ and B‐cell responses in lung parenchyma and airway. Rv3615c contains a dominant epitope of mouse CD4+ T cells, Rv3615c41‐50, and elicits CD4+ T‐cell response with an effector–memory phenotype and multi‐Th1‐type cytokine coexpressions. Since T cells resident at mucosal tissue are potent at control of infection at early stage, our data show that intranasal immunization with Rv3615c promotes a sustained regional immunity to M.tb, and suggests a potency in control of M.tb infection. Our study warranties a further investigation of Rv3615c as a candidate for development of effective vaccination against M.tb infection. 相似文献
8.
Adoptive transfer of CD3+ T cells and CD4+CD44high memory T cells induces autoimmune pancreatitis in MRL/MpJ mice
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Luise Ehlers Sarah Rohde Saleh Ibrahim Robert Jaster 《Journal of cellular and molecular medicine》2018,22(4):2404-2412
The immunopathogenesis of autoimmune pancreatitis (AIP) is poorly understood. Here, we have used MRL/MpJ mice, a model of spontaneous AIP, to address the role of cellular autoimmune processes in the initiation and progression of the disease. Therefore, different T cell subpopulations were adoptively transferred from sick to still healthy (but susceptible) MRL/MpJ mice. Unpurified splenocytes and CD3+ T cells both efficiently induced AIP, while CD4+ and CD8+ T cells alone, as well as splenocytes from healthy mice, were insufficient to trigger the disease. Strikingly, CD4+CD44high memory T cells, although transferred at lower numbers than other T cells, also induced AIP in recipient mice. Employing a modified experimental design, we also evaluated the effects of regulatory T cells (Tregs) on the progression of AIP in already diseased mice. Under the given experimental conditions, there was no significant suppressive effect of adoptively transferred Tregs on pancreatic histopathology. The results of our studies suggest a key role of T cell‐mediated processes in murine AIP. The effects of CD4+CD44high memory T cells are in accordance with genetic studies of our group, which had previously implicated this cell type into the pathogenesis of AIP. In follow‐up studies, we will focus on the interplay of cellular and humoral autoimmunity in the context of AIP. 相似文献
9.
10.
Role of T‐bet,the master regulator of Th1 cells,in the cytotoxicity of murine CD4+ T cells
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Koji Eshima Kana Misawa Chihiro Ohashi Kazuya Iwabuchi 《Microbiology and immunology》2018,62(5):348-356
11.
Peter Lamprecht Anika Erdmann Antje Mueller Elena Csernok Eva Reinhold-Keller Konstanze Holl-Ulrich Alfred C Feller Hilke Bruehl Wolfgang L Gross 《Arthritis research & therapy》2002,5(1):R25-7
Memory T cells display phenotypic heterogeneity. Surface antigens previously regarded as exclusive markers of naive T cells, such as L-selectin (CD62L), can also be detected on some memory T cells. Moreover, a fraction of CD45RO+ (positive for the short human isoform of CD45) memory T cells reverts to the CD45RA+ (positive for the long human isoform of CD45) phenotype. We analyzed patients with biopsy-proven localized Wegener's granulomatosis (WG) (n = 5), generalized WG (n = 16) and age- and sex-matched healthy controls (n = 13) to further characterize memory T cells in WG. The cell-surface expression of CD45RO, CD45RA, CD62L, CCR3, CCR5 and CXCR3 was determined on blood-derived T cells by four-color flow cytometric analysis. The fractions of CCR5+ and CCR3+ cells within the CD4+CD45RO+ and CD8+CD45RO+ memory T cell populations were significantly expanded in localized and generalized WG. The mean percentage of Th1-type CCR5 expression was higher in localized WG. Upregulated CCR5 and CCR3 expression could also be detected on a fraction of CD45RA+ T cells. CD62L expression was seen on approximately half of the memory T cell populations expressing chemokine receptors. This study demonstrates for the first time that expression of the inducible inflammatory chemokine receptors CCR5 and CCR3 on CD45RO+ memory T cells, as well as on CD45RA+ T cells ('revertants'), contributes to phenotypic heterogeneity in an autoimmune disease, namely WG. Upregulated CCR5 and CCR3 expression suggests that the cells belong to the effector memory T cell population. CCR5 and CCR3 expression on CD4+ and CD8+ memory T cells indicates a potential to respond to chemotactic gradients and might be important in T cell migration contributing to granuloma formation and vasculitis in WG. 相似文献
12.
Lymphocytes use the integrin leukocyte function‐associated antigen‐1 (LFA‐1) to cross the vasculature into lymph nodes (LNs), but it has been uncertain whether their migration within LN is also LFA‐1 dependent. We show that LFA‐1 mediates prolonged LN residence as LFA‐1?/? CD4 T cells have significantly decreased dwell times compared with LFA‐1+/+ T cells, a distinction lost in hosts lacking the major LFA‐1 ligand ICAM‐1. Intra‐vital two‐photon microscopy revealed that LFA‐1+/+ and LFA‐1?/? T cells reacted differently when probing the ICAM‐1‐expressing lymphatic network. While LFA‐1+/+ T cells returned to the LN parenchyma with greater frequency, LFA‐1?/? T cells egressed promptly. This difference in exit behaviour was a feature of egress through all assessed lymphatic exit sites. We show that use of LFA‐1 as an adhesion receptor amplifies the number of T cells returning to the LN parenchyma that can lead to increased effectiveness of T‐cell response to antigen. Thus, we identify a novel function for LFA‐1 in guiding T cells at the critical point of LN egress when they either exit or return into the LN for further interactions. 相似文献
13.
Al-Bader T Jolley KA Humphries HE Holloway J Heckels JE Semper AE Friedmann PS Christodoulides M 《Cellular microbiology》2004,6(7):651-662
The major porin proteins present in the outer membrane of Neisseria meningitidis, the causative agent of life‐threatening meningitis and septicaemia, are believed to have potent immunostimulatory effects. In this study, the interactions between human monocyte‐derived dendritic cells (mo‐DC) and the PorA porin were investigated, in order to reveal the role of this protein in promoting innate and adaptive immune responses. Recombinant (r)PorA induced mo‐DC maturation, as reflected by reduced receptor‐mediated endocytosis, increased production of the chemokines IL‐8, RANTES, MIP‐1α and MIP‐1β and augmented expression of the surface markers CD40, CD54, CD80, CD86 and major histocompatibility complex class II molecules. However, rPorA induced either low level or no significant secretion of pro‐inflammatory cytokines from mo‐DC. The protein potently augmented the capacity of mo‐DC to activate both allogeneic CD4+ memory T‐cells and CD4+RA+ naïve T‐cells. In addition, rPorA appeared to inhibit the production of IL‐12p70 that follows from the interaction between CD40 on the mo‐DC and CD40‐ligand on T‐cells, thereby directing T‐cell differentiation towards a Th2 type response. These data demonstrate that PorA is involved in DC activation and in influencing the nature of the T‐helper immune response, which are important properties for generating antibody responses required for protective immunity against meningococci and for determining the immuno‐adjuvant effects of this protein. 相似文献
14.
Cyclin D2 and the CDK substrate p220NPAT are required for self‐renewal of human embryonic stem cells
Klaus A. Becker Prachi N. Ghule Jane B. Lian Janet L. Stein Andre J. van Wijnen Gary S. Stein 《Journal of cellular physiology》2010,222(2):456-464
Self‐renewal of pluripotent human embryonic stem (hES) cells utilizes an abbreviated cell cycle that bypasses E2F/pRB‐dependent growth control. We investigated whether self‐renewal is alternatively regulated by cyclin/CDK phosphorylation of the p220NPAT/HiNF‐P complex to activate histone gene expression at the G1/S phase transition. We show that cyclin D2 is prominently expressed in pluripotent hES cells, but cyclin D1 eclipses cyclin D2 during differentiation. Depletion of cyclin D2 or p220NPAT causes a cell cycle defect in G1 reflected by diminished phosphorylation of p220NPAT, decreased cell cycle dependent histone H4 expression and reduced S phase progression. Thus, cyclin D2 and p220NPAT are principal cell cycle regulators that determine competency for self‐renewal in pluripotent hES cells. While pRB/E2F checkpoint control is relinquished in human ES cells, fidelity of physiological regulation is secured by cyclin D2 dependent activation of the p220NPAT/HiNF‐P mechanism that may explain perpetual proliferation of hES cells without transformation or tumorigenesis. J. Cell. Physiol. 222: 456–464, 2010. © 2009 Wiley‐Liss, Inc. 相似文献
15.
Impact of dose,route, and composition on the immunogenicity of immune polyelectrolyte multilayers delivered on gold templates
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Peipei Zhang James I. Andorko Christopher M. Jewell 《Biotechnology and bioengineering》2017,114(2):423-431
Biomaterial vaccines offer new capabilities that can be exploited for both infectious disease and cancer. We recently developed a novel vaccine platform based on self‐assembly of immune signals into immune polyelectrolyte multilayers (iPEMs). These iPEM vaccines are electrostatically assembled from peptide antigens and nucleic acid‐based toll‐like receptor agonists (TLRas) that serve as molecular adjuvants. Gold nanoparticles (AuNPs) coated with iPEMs stimulate effector cytokine secretion in vitro and expand antigen‐specific T cells in mice. Here we investigated how the dose, injection route, and choice of molecular adjuvant impacts the ability of iPEMs to generate T cell immunity and anti‐tumor response in mice. Three injection routes—intradermal, subcutaneous, and intramuscular—and three iPEM dosing levels were employed. Intradermal injection induced the most potent antigen‐specific T cell responses and, for all routes, the level of response was dose‐dependent. We further discovered that these vaccines generate durable memory, indicated by potent, antigen‐specific CD8+ T cell recall responses in mice challenged with vaccine 49 days after a prime‐boost immunization regimen. In a common exogenous antigen melanoma model, iPEM vaccines slowed or stopped tumor growth more effectively than equivalent ad‐mixed formulations. Further, iPEMs containing CpG—a TLR9a—were more potent compared with iPEMs containing polyIC, a TLR3a. These findings demonstrate the ability of iPEMs to enhance response to several different classes of vaccine cargos, supporting iPEMs as a simple vaccine platform that mimics attractive features of other nanoparticles using immune signals that can be self‐assembled or coated on substrates. Biotechnol. Bioeng. 2017;114: 423–431. © 2016 The Authors. Biotechnology and Bioengineering Published by Wiley Periodicals, Inc. 相似文献
16.
Phenotypic characteristics of aged CD4+ CD28null T lymphocytes are determined by changes in the whole‐genome DNA methylation pattern
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Beatriz Suarez‐Álvarez Ramón M. Rodríguez Karin Schlangen Aroa Baragaño Raneros Leonardo Márquez‐Kisinousky Agustín F. Fernández Carmen Díaz‐Corte Ana M. Aransay Carlos López‐Larrea 《Aging cell》2017,16(2):293-303
Aging is associated with a progressive loss of the CD28 costimulatory molecule in CD4+ lymphocytes (CD28null T cells), which is accompanied by the acquisition of new biological and functional properties that give rise to an impaired immune response. The regulatory mechanisms that govern the appearance and function of this cell subset during aging and in several associated inflammatory disorders remain controversial. Here, we present the whole‐genome DNA methylation and gene expression profiles of CD28null T cells and its CD28+ counterpart. A comparative analysis revealed that 296 genes are differentially methylated between the two cell subsets. A total of 160 genes associated with cytotoxicity (e.g. GRZB, TYROBP, and RUNX3) and cytokine/chemokine signaling (e.g. CX3CR1, CD27, and IL‐1R) are demethylated in CD28null T cells, while 136 de novo‐methylated genes matched defects in the TCR signaling pathway (e.g. ITK, TXK, CD3G, and LCK). TCR‐landscape analysis confirmed that CD28null T cells have an oligo/monoclonal expansion over the polyclonal background of CD28+ T cells, but feature a Vβ family repertoire specific to each individual. We reported that CD28null T cells show a preactivation state characterized by a higher level of expression of inflammasome‐related genes that leads to the release of IL‐1β when activated. Overall, our results demonstrate that CD28null T cells have a unique DNA methylation landscape, which is associated with differences in gene expression, contributing to the functionality of these cells. Understanding these epigenetic regulatory mechanisms could suggest novel therapeutic strategies to prevent the accumulation and activation of these cells during aging. 相似文献
17.
Sun L Hurez VJ Thibodeaux SR Kious MJ Liu A Lin P Murthy K Pandeswara S Shin T Curiel TJ 《Aging cell》2012,11(3):509-519
Regulatory T cells (Tregs) are specialized CD4+ T lymphocytes helping defend against autoimmunity and inflammation. Although age is associated with increased inflammation and autoimmunity, few reports address age effects of immune regulation or auto‐aggressive T cells. We show here that young and aged naïve CD4+ T cells are equivalently auto‐aggressive in vivo in T cell‐driven autoimmune colitis. Young and aged CD4+ Tregs equally suppressed age‐matched T cell proliferation in vitro and controlled clinical and pathologic T cell‐driven autoimmune colitis, suggesting equivalent regulatory function. However, whereas young and aged CD4+ Tregs suppressed interferon (IFN)‐γ+ T cells equivalently in this model, aged CD4+ Tregs unexpectedly failed to restrain interleukin (IL)‐17+ T cells. Nonetheless, young and aged CD4+ Tregs equally restrained IL‐17+ T cells in vivo during acute inflammation, suggesting a chronic inflammation‐related defect in aged CD4+ Tregs. In support, aged Tregs expressed reduced STAT3 activation, a defect associated with poor IL‐17‐producing T cell restraint. Aged naïve mice had markedly increased programmed death (PD)‐1+ T cells, but these exhibited no significant auto‐aggressive or regulatory functions in T cell‐driven colitis. Young CD8+ CD122? T cells induce autoimmune bone marrow failure, but we show that aged CD8+ CD122? T cells do not. These data demonstrate no apparent age‐related increase in auto‐aggressive T cell behavior, but disclose previously unrecognized functional defects in aged CD4+ Tregs during chronic inflammation. IL‐17 can be inflammatory and contributes to certain autoimmune disorders. Reduced aged Treg function during chronic inflammation and reduced IL‐17 restraint could contribute to age‐related inflammation or autoimmunity. 相似文献
18.
Abstract. Objectives: Stem cell antigen 2 (SCA2), also known as TSA1 and LY6E, is a glycosylphosphatidylinositol‐anchored molecule that belongs to the Ly‐6 family and whose function remains largely unknown. We have previously shown that SCA2 is overexpressed in self‐renewing avian erythroid progenitors (T2ECs) as opposed to differentiating T2ECs. The aim of this study was to define the role of SCA2 in the switch between self‐renewal and differentiation of erythroid progenitors. Materials and methods: We have investigated the cellular processes controlled by SCA2 in T2ECs by RNA interference and overexpression approaches. Moreover, we have used a SAGE Querying and analysis tools developed in our laboratory, to investigate the expression level of SCA2 gene in different human cell types. Results: We demonstrate the regulation of SCA2 expression by TGF‐β, a growth factor essential for self‐renewal of T2ECs. We establish that SCA2 knockdown by RNA interference reduced the proliferation and promoted the differentiation of T2ECs. In contrast, SCA2 overexpression inhibited differentiation of T2ECs only. Furthermore, by using a bioinformatic approach, we found that SCA2 is highly expressed in a variety of human cancer cells. We confirmed this result by quantitative PCR on human colon and kidney tissues. Conclusions: Altogether, these findings imply that SCA2 may function in a dose‐dependent manner to support the self‐renewal state and that its deregulation might contribute to the development of some human cancers. 相似文献
19.
Healthcare monitoring systems can provide important health state information by monitoring the biomechanical parameter or motion of body segments. Triboelectric nanogenerators (TENGs) as self‐powered motion sensors have been developed rapidly to convert external mechanical change into electrical signal. However, research effort on using TENGs for multiaxis acceleration sensing is very limited. Moreover, TENG has not been demonstrated for rotation sensing to date. Herein, for the first time, a 3D symmetric triboelectric nanogenerator‐based gyroscope ball (T‐ball) with dual capability of energy harvesting and self‐powered sensing is proposed for motion monitoring including multiaxis acceleration and rotation. The T‐ball can harvest energy under versatile scenarios and function as self‐powered 3D accelerometer with sensitivity of 6.08, 5.87, and 3.62 V g ?1 . Furthermore, the T‐ball can serve as a self‐powered gyroscope for rotation sensing with sensitivity of 3.5 mV so?1. It shows good performance in hand motion recognition and human activity state monitoring applications. The proposed T‐ball as a self‐powered gyroscope for advanced motion sensing can pave the way to a self‐powered, more accurate, and more complete motion monitoring system. 相似文献
20.
Nicola Hoppmann René Gollan Patrick Belikan Julia Bruttger Jérôme Birkenstock Steffen Jung Enric Esplugues Nir Yogev Richard A Flavell Tobias Bopp Frauke Zipp 《The EMBO journal》2016,35(1):89-101
Multiple sclerosis is the most frequent chronic inflammatory disease of the CNS. The entry and survival of pathogenic T cells in the CNS are crucial for the initiation and persistence of autoimmune neuroinflammation. In this respect, contradictory evidence exists on the role of the most potent type of antigen‐presenting cells, dendritic cells. Applying intravital two‐photon microscopy, we demonstrate the gatekeeper function of CNS professional antigen‐presenting CD11c+ cells, which preferentially interact with Th17 cells. IL‐17 expression correlates with expression of GM‐CSF by T cells and with accumulation of CNS CD11c+ cells. These CD11c+ cells are organized in perivascular clusters, targeted by T cells, and strongly express the inflammatory chemokines Ccl5, Cxcl9, and Cxcl10. Our findings demonstrate a fundamental role of CNS CD11c+ cells in the attraction of pathogenic T cells into and their survival within the CNS. Depletion of CD11c+ cells markedly reduced disease severity due to impaired enrichment of pathogenic T cells within the CNS. 相似文献