Academic literature on the topic 'Cellule TFH'
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Journal articles on the topic "Cellule TFH"
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Filho, José Dantas Ribeiro, Paulo Vinícius de Morais Santos, Samuel Rodrigues Alves, et al. "Effects of time and temperature on blood gas and electrolytes in equine venous blood." Acta Veterinaria Brno 89, no. 3 (2020): 239–46. http://dx.doi.org/10.2754/avb202089030239.
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This study aimed to evaluate the viability time of horse venous blood samples kept at laboratory temperature (LT) and in water with ice (WI), to perform blood gas analysis. Eleven blood samples were collected in duplicates from 10 healthy horses. The samples were transported to the laboratory and subjected to one of the 24 h storage method. Each pair of syringes was distinctly kept at LT or submerged in WI. Blood gas tests were performed at times T0h, T1h, T2h, T3h, T4h, T5h, T6h, T8h, T10h, T12h and T24h after collection. Analyses of electrolytes were also performed from the same samples. A difference in blood pH was found between the treatments (P < 0.05). From T4h, pH decreased in samples kept at LT, but in WI, pH did not change. For partial pressure of carbon dioxide (pCO2), a difference between treatments (P < 0.05) was noted starting at T8h. In samples kept at LT, pCO2 increased; no changes occurred in samples stored in WI. There was a decrease in the base concentration beginning at T5h in samples kept at LT (P < 0.05), but no variation in samples kept in WI. These changes can be attributed to the erythrocyte metabolism, still active in vitro, which generates lactic acid from anaerobic glycolysis. The potassium concentration increased in samples kept in WI from T4h, with a gradual increase until T24h. Conservation of equine venous blood samples in WI is efficient in reducing cellular metabolism, thereby increasing the viability of samples for examination and interpretation of results.
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Vaca, Alicia, Mariela Sivina, Karen Clise-Dwyer, et al. "Expansion of T Helper Cell Subsets in Chronic Lymphocytic Leukemia Cell Co-Cultures with Nurselike Cells." Blood 134, Supplement_1 (2019): 1746. http://dx.doi.org/10.1182/blood-2019-125827.
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Background: In secondary lymphatic organs (SLO), chronic lymphocytic leukemia (CLL) cells form characteristic pseudo-follicles, also called proliferation centers, in which proliferating CLL cells are in intimate contact with CD4+ T helper cells. Despite evidence for a co-evolution of CLL cells and counterpart T helper cells, the prevalence and dynamics of T cell subsets, such as T follicular helper cells (TFH), T regulatory helper cells (TRegs) and IL-17-producing T helper cells (Th17) has not been characterized in detail. The CLL nurselike cell (NLC) model recapitulates key cellular and molecular interactions between CLL cells and the microenvironment in SLO, based on functional and gene expression studies, and represents a valid in vitro model for the SLO microenvironment in CLL. To gain insight into the potential role of T cells in CLL SLO, we utilized the NLC model to characterize T helper cell subsets and their dynamics in NLC co-cultures. Methods and Results: First, we quantified CD4+ and CD8+ T cell subsets in fresh peripheral blood mononuclear cell (PBMC) samples from 14 patients and then placed 1x107 PBMCs/ml in culture to establish NLC. We rechecked the relative proportion of CD4+ and CD8+ T cells, as well as absolute T cell counts, and their viability after 3, 6, 9, 12 and 14 days in NLC co-culture conditions. Interestingly, throughout the 14 days of culture, the number of T helper cells remained stable when compared to baseline samples. Next, we characterized T helper cell subsets in 25 different CLL samples, comparing CD4+ T cell subsets in freshly isolated CLL PBMC with matched samples harvested after 14 days of NLC culture. Samples were stained with subset-specific fluorescence-labeled antibody combinations, and analyzed by flow cytometry. NLC co-culture resulted in a significant expansion of TFH and TReg cells. TFH absolute cell counts assessed by flow cytometry using counting beads, increased from 9.4±2.2/μl at baseline to 29.0±5.9/μl in NLC co-cultures (n=14, p=0.001) and TReg from 17.0±3.3/μl to 51.0±15.0/μl (n=14, p=0.027). In contrast, Th17 absolute cell counts declined after 14 days of culture from 113.0±21.0/μl to 68.0±13.0/μl (n=14, p=0.001). Moreover, TH2 cells declined from 42.0±7.4/μl to 30.0±8.2/μl (n=14, p=0.005). Next, we analyzed for changes in TFH subsets (TFH1, TFH2 and TFH17). When compared to TFH cells from CLL PBMC, NLC culture resulted in a relative increase in TFH2 from 17.0±2.4% to 26.0±1.7% (n=25, p=0.013), and in TFH17 from 12.0±1.6% to 21.0±2.7% (n=25, p=0.006) In contrast, TFH1 frequency decreased after 14 days of culture (54.0±3.5% versus 34.0±2.9%, n=25, p=0.001). T follicular regulatory (TFr) cells also increase under co-culture conditions from undetectable to 4.8±1.9% (n=25, p=0.025)(Figure1). Looking at the maturity of CD4+ cells we noted a relative increase of central memory cells from 42.0±3.2% to 50.0±3.2% (n=25, p=0.023), whereas effector memory cells decreased from 34.0±3.4% to 26.0±2.7% (n=25, p=0.009), the fraction of naïve CD4+ cells remained unchanged. Next, we assessed the activation status of co-inhibitory receptors on CD3+CD4+ cells. We found a significant relative increase in CD4+ T cells expressing PD1 and CTLA-4 after 14 days of culture. Additionally, the TFH and TReg subsets demonstrated a significantly higher CTLA-4 expression after culture while TReg cells also addressed an increase in PD1 frequency. Furthermore, we observed a significantly higher CD28 expression on TFH and TReg subsets after 14 days of co-culture. Following, to address the residence and migration capacity of T cells in NLC co-cultures, we analyzed the CD69 and CD62L expression. Our results revealed significantly higher expression of CD69 in NLC co-cultures, whereas CD62L levels remained unchanged. Conclusion: The expansion of TFH and TReg cells in NLC co-cultures suggests the selection and clonal expansion of T cells that may support and engage in crosstalk with CLL cells. Additionally, the expansion of TFr and TFH17 cells could reflect a milieu of immune tolerance establishing in NLC co-cultures. Ongoing TCR sequencing of serial CD4+ T cell samples (baseline versus 14 days under NLC conditions) will characterize changes of clonal architecture in the T helper cell compartment, and will further improve our understanding of co-evolution of CLL and T helper cells. Disclosures Wierda: Gilead Sciences: Research Funding; Juno Therapeutics: Research Funding; KITE pharma: Research Funding; Sunesis: Research Funding; Miragen: Research Funding; Janssen: Research Funding; Xencor: Research Funding; Acerta Pharma Inc: Research Funding; Pharmacyclics LLC: Research Funding; Genentech: Research Funding; AbbVie: Research Funding; GSK/Novartis: Research Funding; Oncternal Therapeutics Inc.: Research Funding; Cyclcel: Research Funding; Loxo Oncology Inc.: Research Funding. Burger:Aptose Biosciences, Inc: Research Funding; BeiGene: Research Funding; Gilead Sciences: Research Funding; AstraZeneca: Honoraria; Janssen Pharmaceuticals: Consultancy, Honoraria; Pharmacyclics, an AbbVie company: Research Funding.
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DiToro, Daniel F., Colleen J. Winstead, Rakieb Andargachew, et al. "IL2 production predicts Tfh differentiation." Journal of Immunology 198, no. 1_Supplement (2017): 150.18. http://dx.doi.org/10.4049/jimmunol.198.supp.150.18.
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Abstract Naïve CD4 T cells differentiate into functionally distinct subsets in response to a set of extrinsic and intrinsic cues. Effector subsets, including Th1, Th2 and Th17 CD4s, are required for optimal cellular responses to invading pathogens, while class switched antibody responses depend on the differentiation of T follicular helper cells (Tfh). Development of both Tfh and non-Tfh occurs in parallel and involves two distinct but functionally related expression bifurcations. Upon formation of T cell receptor (TCR)/major histocompatibility (MHC) synapses with antigen-presenting cells (APC), a discrete subset of activated T cells secretes the cytokine IL2. Similarly, a portion of activated cells express the transcription factor Bcl6 and differentiate into Tfh cells, while the remainder express Blimp1 and develop into effector CD4s. However, the cellular, temporal and mechanistic relationships between these two bifurcations remain unclear. Here we show that the IL2 and Bcl6/Blimp1 expression bifurcations occur simultaneously, precede cell division, predict differentiation into Tfh and non-Tfh subsets, and are mechanistically related to antigen availability TCR density.
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Choi, Seung-Chul, Anton Titov, Georges Abboud, and Laurence Morel. "Autoreactive and immunization-induced follicular helper T cells have opposite glucose and glutamine requirements." Journal of Immunology 200, no. 1_Supplement (2018): 163.7. http://dx.doi.org/10.4049/jimmunol.200.supp.163.7.
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Abstract Both glycolysis and mitochondrial oxidative metabolism are elevated in CD4+ T cells from lupus-prone mice, and metabolic inhibitors targeting both of these pathways normalized lupus T cell functions in vitro and reverted disease in mice. Here, we showed that inhibiting glucose metabolism with 2-deoxy-D-glucose (2DG) results in a drastic reduction of follicular helper T (TFH) cell frequency in lupus-prone B6.Sle1.Sle2.Sle3 (TC) mice. However, treatment of TC mice with 2DG had little effect on the production of antibodies or the expansion of TFH cells following immunization with a nominal antigen of T-cell-dependent (TD) humoral responses, and no effect on the frequency of influenza virus-specific TFH cells induced by immunization with PR8 influenza virus. Thus, TFH cells supporting the production of autoantibodies are different from TFH cells providing protective humoral immunity against pathogens. The specific metabolic signature from autoimmune TFH cell is significantly different compared with exogenous antigen-specific TFH cells. Further results obtained with gene expression analysis and treatment with metabolic inhibitors indicated that autoreactive TFH cells depend on glucose metabolism, while exogenous antigen-specific TFH cells are more glutamine-demanding. Overall, our results predict that targeting TFH cellular metabolism provides an effective and safe therapeutic approach for systemic autoimmunity by eliminating autoreactive TFH cells.
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Padhan, Kartika, Eirini Moysi, Alessandra Noto, et al. "Acquisition of optimal TFH cell function is defined by specific molecular, positional, and TCR dynamic signatures." Proceedings of the National Academy of Sciences 118, no. 18 (2021): e2016855118. http://dx.doi.org/10.1073/pnas.2016855118.
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The development of follicular helper CD4 T (TFH) cells is a dynamic process resulting in a heterogenous pool of TFH subsets. However, the cellular and molecular determinants of this heterogeneity and the possible mechanistic links between them is not clear. We found that human TFH differentiation is associated with significant changes in phenotypic, chemokine, functional, metabolic and transcriptional profile. Furthermore, this differentiation was associated with distinct positioning to follicular proliferating B cells. Single-cell T cell receptor (TCR) clonotype analysis indicated the transitioning toward PD-1hiCD57hi phenotype. Furthermore, the differentiation of TFH cells was associated with significant reduction in TCR level and drastic changes in immunological synapse formation. TFH synapse lacks a tight cSMAC (central supra molecular activation Cluster) but displays the TCR in peripheral microclusters, which are potentially advantageous in the ability of germinal center (GC) B cells to receive necessary help. Our data reveal significant aspects of human TFH heterogeneity and suggest that the PD-1hiCD57hi TFH cells, in particular, are endowed with distinctive programming and spatial positioning for optimal GC B cell help.
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Zander, Ryan A., Gang Xin, David Schauder, and Weiguo Cui. "T follicular helper cell-derived IL-10 sustains humoral immunity during chronic viral infection." Journal of Immunology 198, no. 1_Supplement (2017): 122.2. http://dx.doi.org/10.4049/jimmunol.198.supp.122.2.
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Abstract Although it is well-appreciated that Tfh cells play a critical role in regulating antiviral humoral immunity, the detailed cellular and molecular pathways that govern their differentiation and function during chronic viral infection remains incompletely understood. In this study, we generated IL-10 and IL-21 double-reporter mice to study the dynamic expression of the immunoregulatory cytokines IL-10 and IL-21, which are known to differentially regulate T cell-mediated control over viral replication. Infection of these double-reporter mice with either an acute or chronic strain of LCMV, revealed a unique subset of IL-10+IL-21+co-producing Tfh cells that arise only during chronic viral infection. Notably, compared to IL-21-single producing Tfh cells, IL-10+IL-21+co-producing Tfh cells exhibited an enhanced germinal center (GC) Tfh-like profile, as exemplified by their increased per cell expression of PD-1, CXCR5, and Bcl-6. Additional analyses identified that IL-10-producing Tfh cells have an increased capacity to form stable Tfh-B cell conjugates compared to their IL-10− Tfh counterparts, suggesting that IL-10+ Tfh cells may specialize in providing help signals to B cells during chronic infection. Importantly, depletion of IL-10+IL-21+ co-producing CD4 T cells or deletion of Il10 specifically from Tfh cells resulted in impaired GC B cell responses, LCMV-specific antibody production and viral control. Mechanistically, we show that B cell intrinsic IL-10 signaling is indispensable for GC B cell differentiation and function. Collectively, our findings delineate a heterogeneous population of Tfh cells and elucidate a critical role for Tfh-derived IL-10 in promoting humoral immunity during persistent viral infection.
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Houser, Cassandra L. "Aryl hydrocarbon receptor regulation of T follicular helper cells during respiratory viral infection." Journal of Immunology 206, no. 1_Supplement (2021): 24.02. http://dx.doi.org/10.4049/jimmunol.206.supp.24.02.
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Abstract The aryl hydrocarbon receptor (AHR) is a ligand-regulated transcription factor that binds structurally diverse molecules from the environment, including pollutants, dietary factors, and chemicals from microorganisms. AHR-binding compounds alter adaptive immune responses, but the cellular components affected and governing mechanisms are not fully defined. For instance, AHR activation affects antibody responses; a process for which T follicular helper cells (Tfh cells) are critical. We recently discovered that AHR activation alters the percentage and number of Tfh cells during influenza A virus (IAV) infection. Yet, how the AHR modulates Tfh cells is not known. The present work shows that AHR-mediated changes to Tfh cells are due to changes in CD4+ T cell proliferation and BCL6 expression, an essential transcription factor for Tfh cell differentiation. Utilizing conditional AHR knockout mice, we show that changes to Tfh cells require AHR expression in CD4+ T cells. The AHR regulates gene expression directly, via its DNA-binding domain (DBD), and indirectly via other signaling molecules. To delineate which pathways it uses to modulate Tfh cells, we used mice with a mutated AHR DBD and demonstrate that it requires its cognate DBD to regulate Tfh cells during infection. This supports that AHR modulates Tfh cells by directly regulating gene expression. Overall, these findings provide new information about how AHR signaling influences humoral immunity to a common respiratory pathogen. Given that exposure to AHR-binding pollutants impacts immune responses to infections and vaccines, better understanding of the mechanisms that control Tfh cell responses has broad reaching impact on immune defenses and immune-mediated diseases.
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Petrovas, Constantinos, Takuya Yamamoto, Michael Gerner, et al. "Increased immune activation during chronic SIV infection drives the TFH dynamics. (105.33)." Journal of Immunology 188, no. 1_Supplement (2012): 105.33. http://dx.doi.org/10.4049/jimmunol.188.supp.105.33.
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Abstract We have investigated the phenotype, location, molecular signature and function of follicular CD4 T helper cells (TFH) in rhesus macaques. Similar to human TFH, they are characterized by a CCR7lowPD-1highICOShighCTLA-4highCXCR4high phenotype and represent a heterogeneous population with respect to cytokine function. PD-1high CD4 cells were localized closer to the follicle center than PD-1low CD4 cells. This relative cellular distribution was not affected by the SIV infection. Production of Th1 cytokines was compromised while IL-4 was secreted predominantly by a highly differentiated (CD150low) subpopulation of TFH cells. Compared to non-TFH cells, TFH cells exhibited a distinct gene profile that was significantly altered by SIV infection. A significant reduction in the expression of the IL-4 gene in TFH was found implying a defective help for the development of B cell responses during chronic SIV. CD150low TFH cells were characterized by defective survival while in vivo BrdU integration studies revealed a defective cycling capacity of these cells. Preferential infection of TFH cells was found only during acute SIV yet progression to chronic SIV resulted in their accumulation, which was associated with high immune activation and altered IL-6-induced signaling. Thus, the preservation of TFH in the face of high rates of infection can be explained by their normally short half-life and the diverse populations of CD4 T cells that can provide to their continual replenishment.
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Kang, Seung Goo, Wen-Hsien Liu, John Teijaro, et al. "MiR-17~92 family microRNAs are critical regulators of T follicular helper cell differentiation (P1133)." Journal of Immunology 190, no. 1_Supplement (2013): 50.9. http://dx.doi.org/10.4049/jimmunol.190.supp.50.9.
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Abstract Germinal center (GC) reaction is a key event in B cell-mediated immune responses and CD4+ T cell help plays an essential role in these process. A distinct CD4+ effector T cell subset, T follicular helper cells (TFH), provides this help to B cells. However, molecular mechanisms underlying TFH differentiation are still largely unknown. A recent study revealed that Bcl-6 is a signature transcription factor regulating TFH differentiation and it represses the expression of miR-17~92 in CD4+ T cells. MiR-17~92 in turn suppresses the expression of CXCR5, a critical chemokine receptor controlling CD4+ T cell migration into B cell follicles. The authors therefore concluded that miR-17~92 functions as a negative regulator of TFH differentiation. Here we report the surprising finding that mice with miR-17~92 family microRNAs (miRNAs) deleted specifically in T cells exhibited severely compromised TFH differentiation, germinal center formation, and reduced antibody responses upon protein antigen immunization. Those mutant mice were also defective in TFH differentiation and germinal center B (GCB) cell formation during lymphocytic choriomeningitis virus (LCMV) clone-13 infection and failed to control the virus. Conversely, T cell-specific miR-17~92 transgenic mice spontaneously accumulated TFH cells. Novel cellular and molecular mechanisms underlying miR-17~92 family miRNA-mediated regulation of TFH differentiation will be presented at this meeting.
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Liu, Wen-Hsien, Seung Goo Kang, Zhe Huang, et al. "A miR-155–Peli1–c-Rel pathway controls the generation and function of T follicular helper cells." Journal of Experimental Medicine 213, no. 9 (2016): 1901–19. http://dx.doi.org/10.1084/jem.20160204.
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MicroRNA (miRNA) deficiency impairs the generation of T follicular helper (Tfh) cells, but the contribution of individual miRNAs to this phenotype remains poorly understood. In this study, we performed deep sequencing analysis of miRNAs expressed in Tfh cells and identified a five-miRNA signature. Analyses of mutant mice deficient of these miRNAs revealed that miR-22 and miR-183/96/182 are dispensable, but miR-155 is essential for the generation and function of Tfh cells. miR-155 deficiency led to decreased proliferation specifically at the late stage of Tfh cell differentiation and reduced CD40 ligand (CD40L) expression on antigen-specific CD4+ T cells. Mechanistically, miR-155 repressed the expression of Peli1, a ubiquitin ligase that promotes the degradation of the NF-κB family transcription factor c-Rel, which controls cellular proliferation and CD40L expression. Therefore, our study identifies a novel miR-155–Peli1–c-Rel pathway that specifically regulates Tfh cell generation and function.
Dissertations / Theses on the topic "Cellule TFH"
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RIPAMONTI, ANNA. "Ruolo dei microRNA nel differenziamento e funzionalità delle cellule T follicolari umane." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2015. http://hdl.handle.net/10281/83941.
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Le cellule follicolari T helper (TFH) sono una sottopopolazione separata di cellule CD4+ T helper specializzate nel fornire aiuto alle cellule B. Si sviluppano in maniera indipendente dalle altre sottopopolazioni di cellule T e sono fondamentali per l'immunità umorale, compresa la generazione di plasmacellule di lunga durata e ad alta affinità e di cellule B della memoria. Alterazione di geni specifici delle cellule TFH porta a difetti nella formazione dei centri germinativi (GC), con conseguenti disordini autoimmuni o immunodeficienze.
I meccanismi molecolari alla base del differenziamento delle cellule TFH umane sono poco conosciuti. I microRNA (miRNA) sono piccole molecole di RNA non codificanti a singolo filamento e altamente conservati, che controllano l'espressione genica a livello post-trascrizionale legandosi alla regione 3’ non tradotta del mRNA bersaglio. Per studiare il ruolo dei miRNA nella biologia delle cellule TFH abbiamo eseguito RT-qPCR e un’analisi tramite deep-sequencing su cellule TFH e Naive CD4+ T isolate da adenoidi umane. Abbiamo identificato miRNA specifici delle cellule TFH umane e abbiamo convalidato in vitro i loro bersagli molecolari predetti. Abbiamo scoperto che miRNA specifici delle cellule TFH umane regolano trascritti specificamente espressi nella sottopopolazione di cellule TFH e noti per essere essenziali per la loro funzione. Abbiamo eseguito esperimenti di gain o loss-of function utilizzando vettori lentivirali volti a modulare l'espressione dei miRNA in cellule TFH umane. Attraverso questi esperimenti abbiamo valutato come questi miRNA specifici delle cellule TFH umane influenzano la capacità delle cellule TFH di fornire aiuto alle cellule B, e abbiamo chiarito il loro ruolo nella biologia delle cellule TFH.
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Marschall, Pierre. "Etude de la fonction des cellules dendritiques dans la réponse immunitaire cutanée de type 2." Thesis, Strasbourg, 2019. http://www.theses.fr/2019STRAJ044.
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La dermatite atopique (AD) est une des maladies inflammatoires chroniques cutanée les plus fréquentes qui affecte jusqu'à 20% des enfants et 3% des adultes dans le monde. Elle se caractérise par une inflammation chronique de la peau et des réponses immunitaires humorale et de type 2. Mon travail de thèse est d'étudier le rôle des cellules dendritiques (DCs) dans la génération des lymphocytes T et la pathogenèse de l'AD. Dans la partie I, à l'aide de deux modèles murins d'AD, l'un déclenché par la surexpression de TSLP dans la peau induite par l'application topique de MC903 et l'autre par sensibilisation à un allergène à travers une peau dont la barrière épidermique est lésée, nous montrons le rôle crucial joué par TSLP dans la différentiation des lymphocytes T auxiliaires folliculaires (Tfh) et le développement des centres germinatifs (GC). Nous établissons le rôle contradictoire des cellules de Langerhans dans la réponse Tfh/GC promue par TSLP. Dans la partie II, nous montrons que, en plus de son implication dans la réponse Th2, TSLP signale par son récepteur TSLPR à la surface des DCs pour induire la différentiation des lymphocytes Tregs ST2+ dans le ganglion drainant. De plus, la différentiation de ces cellules implique OX40L, molécule de costimulation exprimée par certaines DCs migratoires, suggérant que l'axe TSLP-TSLPRDC-OX40L joue un rôle non reconnu dans l'induction des lymphocytes Tregs ST2+ dans le cadre de l'AD<br>Atopic dermatitis (AD) is a one of the most common chronic inflammatory skin disease which affects up to 20% of children and 3% of adults worldwide, with increasing prevalence in the industrialized countries during the last 30 years. It is characterized by chronic cutaneous inflammation, humoral and T helper type 2 (Th2) responses. My PhD study is to investigate the role of skin dendritic cells (DCs) in the generation of T helper cells in the pathogenesis of AD. In the Part I, using two mouse models of AD, one triggered by the overexpression of TSLP in mouse skin through topical application of MC903, and the other one with epicutaneous allergen sensitization on barrier-disrupted skin, we demonstrated a crucial role of TSLP in promoting T follicular helper (Tfh) cell differentiation and germinal center (GC) response. We uncovered a seemingly contradictory role of Langerhans cells in TSLP-promoted Tfh/GC response. In the part II, we showed that, in addition to promote Th2 cell differentiation, TSLP signals through TSLPR expressed by DCs to induce the differentiation of ST2+ Tregs in skin-draining lymph nodes. Interestingly, the differentiation of these cells implicates OX40L, a costimulatory molecule expressed in a subset of migratory DCs, suggesting a previously unrecognized role of TSLP-TSLPRDC-OX40L axis in the induction of ST2+ Tregs in AD pathogenesis
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Croizet, Karine. "Identification et caractérisation d'une population de cellules dendritiques (DC) dans les cultures primaires de thyrocytes : mise en évidence d'un contrôle des fonctions différenciées des DC par la TSH via les thyrocytes." Lyon 1, 1999. http://www.theses.fr/1999LYO1T200.
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Moukambi, Félicien. "Études de la dynamique des cellules Tfh et T CD4 mémoires au cours de l'infection au VIH." Doctoral thesis, Université Laval, 2017. http://hdl.handle.net/20.500.11794/27740.
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Depuis sa découverte, le virus de l’immunodéficience humaine de type 1 (VIH-1) a causé la mort de 33 millions de personnes, et 36,7 millions sont actuellement infectées. Malgré l’existence des thérapies antirétrovirales, celles-ci ne conduisent pas à d’éradiquer le virus. En outre, il n’existe pas de vaccin. Les lymphocytes B, dont la fonction est de produire les anticorps sont dysfonctionnels au cours du VIH-1. Or la majorité des stratégies vaccinales se basent sur la production d’anticorps dépendante des cellules T CD4. Ainsi, la première partie de mon doctorat a été consacré à la compréhension de l’impact du VIH-1 sur les cellules T CD4 folliculaires auxiliaires (Tfh) essentielles à l’activation des lymphocytes B et à la production d’anticorps spécifiques, dans la rate l’organe majeur de la réponse des lymphocytes B. Dans la deuxième partie, j’ai analysé les cellules T CD4 mémoires, Tfh et les lymphocytes B dans les ganglions mésentériques: un site inducteur de la réponse immunitaire intestinale, qui alimente la lamina propria (site effecteur) de la muqueuse intestinale en cellules mémoires. Étant donné l’impossibilité d’étudier ces organes profonds en particulier en phase aiguë chez l’homme, j’ai utilisé le modèle du macaque rhésus infecté par le virus de l’immunodéficience simienne (VIS). Les résultats de ces études montrent que l’évolution vers le SIDA est associée à une déplétion précoce des cellules Tfh et T CD4 mémoires dans la rate et les ganglions mésentériques. Concomitant à cela, je rapporte une déplétion des lymphocytes B mémoires dans la rate et un faible titre d’IgG anti-VIS dans le sérum. En plus, les cellules Tfh commutent leur phénotype d'effecteur mémoire vers celui de centrale mémoire associé à l’expriment de CD127 (récepteur de l’IL-7) et de T-bet (marqueur de cellules Th1). De plus, je montre que la déstructuration des organes lymphoïdes secondaires, ainsi que les cytokines environnementales comme l’IL-7 ou l’IL-27 peuvent contribuer au dysfonctionnement des cellules Tfh puisque ces dernières induisant les facteurs de transcription inhibiteurs des cellules Tfh tels que T-bet, Foxo1, Stat5 et KLF2. En conclusion, mes résultats permettent de mieux comprendre que le dysfonctionnement des lymphocytes B et l’immunodéficience dans la muqueuse intestinale sont associés à la déplétion soudaine des lymphocytes T CD4 mémoires et Tfh dans la rate et les ganglions mésentériques. Par conséquent, prévenir la perte de ces cellules pourrait être une approche thérapeutique et vaccinale prometteuse pour la neutralisation du virus et pour une meilleure immunité intestinale, afin d’empêcher la translocation bactérienne.<br>Since its discovery, HIV-1 has caused the death of 35 million people, and 36.9 million are living infected. Although researches have led to the development of antiretroviral therapies, which not only improve life expectation but also life quality of infected individuals, these therapies are not capable of eradicating the virus, and unfortunately there is no vaccine. The pathogenesis of HIV-1 is linked to a dysfunction of CD4 T cells that favors progression to AIDS. Therefore, given that most vaccines are based on T cell-dependent antibody production, the first part of my PhD research is devoted to understanding the impact of HIV-1 on CD4 T Follicular helper (Tfh) cells, which are essential for B cell activation and the production of specific antibodies. These cells are particularly crucial in the spleen, which is the major organ for B cell response. In the second part, I have analyzed the dynamics of memory CD4 T, Tfh and of B cells in mesenteric lymph nodes: an inductive site of the immune response that provides memory cells to the lamina propria (effector site) of the intestinal mucosa. Given the difficulties to study these deep organs, particularly during the acute phase in humans, I have used rhesus macaques infected with the simian immunodeficiency virus (SIV) to study the dynamics of Tfh cells. My results show an early depletion of splenic Tfh cells during the acute phase; a depletion that persists during the chronic phase within macaques in which the infection rapidly progresses to AIDS. Concomitantly, we report a depletion of memory B cells and low titers of anti-SIV IgG titers in these macaques. Furthermore, I observed a massive depletion of memory CD4 T, Tfh and B cells in mesenteric lymph nodes, as well as a phenotypic change of Tfh cells that become central memory cells associated with the upregulation of the expression of CD127 (IL-7 receptor). My results also show that environmental cytokines such as IL-7 and IL-27 contribute to their dysfunction as support the expression of transcription factors that inhibit Tfh cells such as T-bet, Foxo1 and Stat5. In conclusion, my results provide a better understanding of B cell dysfunction related to the early loss of the Tfh cells during HIV/SIV infection. Moreover, I hypothesize that the loss of immunity in the intestinal mucosa is due to the sudden depletion of memory CD4 T, Tfh and B cells in the mesenteric lymph nodes. Therefore, maintaining Tfh and memory CD4 T cells during the early phase of infection could be a promising therapeutic and vaccine approach for neutralizing HIV/SIV, as well as preventing bacterial translocation.
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Mary, Romain. "Améliorer les effets anti-tumoraux des lymphocytes T folliculaires helper (Tfh) en ciblant la communication intercellulaire entre Tfh et Th2." Thesis, Bourgogne Franche-Comté, 2019. http://www.theses.fr/2019UBFCI009/document.
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Il est maintenant acquis que le système immunitaire occupe une place importante dans l’évolution les cancers (Hanahan et al., 2011). La compréhension actuelle de la réponse immunitaire adaptative en fait une cible de choix dans ce contexte. Il est apparu que les lymphocytes T CD4+, acteurs majeurs de la composante adaptative du système immunitaire, présentent des actions distinctes sur le contrôle de la croissance tumorale. Ainsi, les lymphocytes Th2 et Tfh, tous deux activateurs des lymphocytes B dans des conditions de lutte contre des infections pathogéniques, présentent des rôles ambivalents dans un contexte de cancer. En effet, de nombreuses études montrent que la présence de Th2 est corrélée à une progression de la maladie (notamment via l’action de l’IL-4 qu’ils sécrètent) (Koller et al., 2010 ; Roca et al., 2012) alors que les Tfh, seraient plutôt associés à un bon pronostic pour les patients (Gu-Trantien et al., 2013, 2017).Nos investigations actuelles nous ont permis de mettre en avant une caractéristique nouvelle de la biologie des lymphocytes Tfh. En effet, les Tfh expriment l’Hemathopoietic Prostaglandin D2 synthase (HPGDS). Cette enzyme de la voie de biosynthèse des eicosanoïdes est responsable de la production de Prostaglandine D2 (PGD2). Plusieurs travaux montrent que les cellules Th2 expriment le récepteur CRTH2, spécifique de la PGD2. Cette molécule agit sur ces cellules comme chemoattractant et permet également une augmentation de leur production cytokinique. Ainsi, nous posons l’hypothèse d’une communication potentielle entre lymphocytes Tfh et Th2 via la PGD2. Le projet présenté ici est alors axé sur la compréhension des mécanismes moléculaires et cellulaires sous-jacent à cette communication au sein des deux sous-types ainsi que sur son impact dans un contexte de cancer. Ce projet ayant également pour but de mettre en avant la PGD2 comme nouvelle cible thérapeutique dans le cancer<br>It is now accepted that the immune system plays a critical role in cancers evolution (Hanahan et al., 2011). In this context, current understanding of the adaptive immune response made it a prime target. T CD4 cells, the main players of the adaptive immune system component, are known to possess distinct roles in the control of tumour growth. Thereby, Th2 and Tfh cells, both known to activate B cells in pathogenic infections, present antagonistic roles in cancer. Indeed, numerous studies demonstrate that Th2 cells are correlated with disease progression (especially via IL-4 secretion) (Koller et al., 2010 ; Roca et al., 2012), whereas Tfh cells are associated with a good prognosis for the patients (Gu-Trantien et al., 2013, 2017) despite the actual limited amount of available data.Our current researches highlighted a new property of the biology of Tfh cells. We found that Tfh cells are able to express the Hemathopoietic Prostaglandin D2 synthase (HPGDS), an eicosanoid pathway enzyme involved in Prostaglandin D2 (PGD2) production. Moreover, different studies revealed that Th2 cells expressed CRTH2, the specific PGD2 receptor. PGD2 is known as a chemoattractant molecule for Th2 cells and lead to the increase of their cytokine secretion. We hypothesized that Tfh communicate with Th2 cells via PGD2 signalling. The present project is focused on the understanding of the underlying molecular and cellular mechanisms involved in this cross-talk and their impact in cancer. The last aim of this work is to favor the development of PGD2 as a new cancer therapeutic target
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Wei, Ruicheng. "Etudes des mécanismes cellulaires et moléculaires de la réponse immunitaire de type 2 dans la dermatite atopique." Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ047.
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Mon travail, lors de ma thèse, avait pour but d’étudier la différentiation des lymphocytes Tfh, ainsi que leur fonction et leur régulation dans la pathogenèse de la DA. Pour cela, j’ai utilisé un modèle murin précédemment établi au sein de notre laboratoire consistant en l’application topique de MC903 (un analogue de la vitamine D3) induisant la production de TSLP par les kératinocytes et, par conséquence, la réponse immunitaire Th2 et la pathogenèse de la DA. mon travail doctoral s’est porté sur la différentiation des lymphocytes Tfh, leur production cytokinique ainsi que la formation des centres germinatifs dans le contexte d’un modèle murin de DA induite par le MC903. Mes études ont démontré un rôle critique joué par TSLP dans la réponse Tfh et ont exploré le rôle potentiellement joué par les cellules dendritiques langerine+ et la signalisation OX40L dans le développement des réponses Tfh et de type 2. Ceci nous a permis d’approfondir nos connaissances concernant les mécanismes sous-tendant la réponse immunitaire de type 2 dans la pathogenèse de la DA. Dans la deuxième partie de ma thèse, nous avons examiné le rôle de MC903 dans la régulation de l’inflammation due au psoriasis, en utilisant un modèle de psoriasis induit par l’Aldara. Nous avons montré que MC903 inhibe l’axe 23/IL-17/IL-22 chez les souris souffrant de psoriasis. De plus, cette inhibition semblait être dose-dépendante. Nous avons en outre exploré le rôle de TSLP et VDR dans la médiation de cet effet dû au MC903<br>My thesis aimed at studying the Tfh cell differentiation, function and regulation in AD pathogenesis. To this aim, I employed our previously established AD mouse model in which MC903 (a vitamin D analog) topical treatment on the skin induces TSLP production bykeratinocytes, promotes Th2 cell response and drives the pathogenesis of AD. my thesis work investigated Tfh cell differentiation, its cytokine expression and germinal center formation using MC903-induced AD mouse model. By exploring the role of TSLP,Langerin+ DCs and OX40L signaling in Tfh cell differentiation and regulation, my study provides novel insights into the mechanisms underlying the type 2 immune response in AD pathogenesis. In the second part of my study, we examined the role of MC903 in regulating the psoriatic inflammation using Aldara-induced psoriasis model. We showed that MC903 inhibited IL-23/IL-17/IL-22 axis in mouse psoriasis. Moreover, this inhibition exhibited a dose-dependent manner. We further explored the role of TSLP and VDR in mediating such effect of MC903
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Bell, Andrea. "TSH signaling and cellular responses in preadipocytes and adipocytes." Thesis, University of Ottawa (Canada), 2004. http://hdl.handle.net/10393/29077.
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Thyroid stimulating hormone (TSH) action in adipose tissue remains largely unknown. We demonstrate that TSH activates protein kinase B (PKB/Akt) and p70 S6 kinase (p70 S6K) in a phosphoinositide 3-kinase (PI3K)-dependent manner in 3T3-L1 preadipocytes. TSH had no effect on cAMP levels, suggesting adenylyl cyclase is not involved in TSH activation of the PI3K-PKB/Akt-p70 S6K pathway. 3T3-L1 preadipocyte cell death was reduced by 29 to 76%, in serum-deprived (6 h) preadipocytes treated with 1--20 muM TSH, respectively. In the presence of 20 muM TSH, an 88% reduction in TUNEL-positive cells was observed in serum-starved (3 h) 3T3-L1 preadipocytes, as well as a 93% reduction in the level of cleaved activated caspase 3. TSH acts as a survival factor for serum-deprived preadipocytes, reducing TUNEL-positive cells and caspase 3 activation. A role for TSH may exist in adipose tissue development and remodeling.
Interleukin-6 (IL-6), a pro-atherogenic cytokine, is expressed and secreted by adipocytes, but little is known about its regulation. Since an elevated TSH serum level is a cardiovascular disease (CVD) risk factor, and since thyroid stimulating hormone receptor (TSHR) is expressed in adipocytes, we investigated whether TSH modulates IL-6 secretion in cultured 3T3-L1 and 3T3-F442A mouse adipocytes, and in primary cultures of human abdominal adipocytes differentiated in culture. TSH increased the secretion of IL-6 by 5-fold in 3T3-F442A adipocytes, by 2-fold in 3T3-L1 adipocytes, and by 3.5-fold in human differentiated adipocytes. TSH is a novel regulator of adipocyte IL-6 secretion, providing a potential mechanism for epidemiological observations identifying an elevated serum TSH level as a CVD risk factor.
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Placek, Katarzyna. "Contrôle épigénétique de la différentiation des cellules Th humaines." Paris 7, 2010. http://www.theses.fr/2010PA077212.
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Dans ce projet nous avons identifié les mécanismes impliqués dans la régulation de l'expression du gène TBET et les changements épigénétiques des locus codant pour les cytokines IL-22, IL-26 et IFN-γ pendant le développement des lymphocytes T auxiliaires (Th) humaines. TBET n'est pas exprimé dans les cellules T naives mais il est induit pendant la différentiation des cellules Thl. Nous avons montré que l'activation des cellules T CD4 induit deux sites hypersensibles à la Dnase I (HS) sur le locus TBET, l'acétylation des histones et l'expression du gène. NFAT activé par TCR est recruté au HS in vivo. IL-12 et IFN-γ ne sont pas suffisant pour induire TBET mais amplifient son expression dans les cellules stimulées par TCR. STAT4 activé par IL-12 est recruté au niveau du troisième HS trouvé dans les cellules Thl. Nous avons montré que les modifications des histones et l'expression du gène TBET sont initiées par NFAT activé en réponse à la stimulation par TCR et sont renforcées par STAT4 activé par IL-12. Ces deux facteurs sont recrutés au niveau de sites distincts sur le locus TBET. Les gènes codants pour les cytokines IL-22 et IL-26 sont localisés à proximité du gène IFNG suggérant leur corégulation. Nous avons trouvé que différentes conditions de stimulation induisent des niveaux d'expression et des niveaux de modifications épigénétiques différentes de ces trois gènes. Les modifications H4ac et H3K4me2 sur les régions régulatrices potentielles de locus IL22/IL26/IFNG sont induites par le TCR et la présence de cytokines peuvent les modifier. L'activation par le TCR n'affecte pas le niveau de PH3K27me3 sur les gènes IL22 et IL26 mais le diminue sur le locus de VIFNG<br>In this work we study of the factors determining the expression of the T-bet gene, the master regulator of Th type 1 (Thl) cell development and epigenetic changes at the IL22/IL26/IFNG locus during Th cell differentiation. T cell activation induced two strong DNAsel hypersensitive sites (HS) and rapid histone acetylation at these elements in CD4+ T cells. Histone acetylation and T-bet expression were strongly inhibited by CsA and NFAT bound to a HS in vivo. IL-12 and IFN-γ signaling alone were not sufficient to induce T-bet in naive CD4+ T cells, but enhanced T-bet expression in TCR-stimulated cells. A third HS 12kb upstream of the mRNA start site in developing Thl cells was bound by IL-12-activated STAT4. Our data suggest that TBET locus remodeling and gene expression are initiated by TCR-induced NFAT recruitment and amplified by IL-12-mediated STAT4 binding to two distinct distal regulatory elements during human Thl cell development. The IL22 and IL26 genes are located close to the Thl-specific IFNG gene, suggesting that these loci may be coregulated. We found that different stimulation conditions induced transcription and different histone modification pattern of these genes. Permissive H4ac and H3K4me2 were strongly induced by TCR during in vitro differentiation of T helper cells. Cytokines may influence the level of these modifications at potential regulatory elements of IL22/IL26/IFNG locus. In contrast, T cell activation by TCR does not influence the level of H3K27me3 at IL22 and IL26 genes but removes H3K27me3 from the INFG locus. These observations suggest that there are different modes regulating expression of these three genes
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Pradet-Balade, Bérengère. "Evolution de la regulation de la fonction thyreotrope : etude chez les teleosteens (doctorat : biochimie et biologie moleculaire)." Paris 11, 1998. http://www.theses.fr/1998PA11T030.
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Rivat, Christine. "Rôle de la signalisation STAT3 dans la progression tumorale des cellules épithéliales coliques." Paris 6, 2004. http://www.theses.fr/2004PA066286.
Full textBook chapters on the topic "Cellule TFH"
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Nistri, A., N. D. Fisher, and G. Baranauskas. "TRH and Substance P Increase Rat Motoneurone Excitability through a Block of a Novel K+ Conductance." In Cellular Mechanisms of Sensory Processing. Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78762-1_16.
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Martiny, L., B. Thuilliez, B. Lambert, F. Antonicelli, C. Jacquemin, and B. Haye. "Control by TSH of the Production by Thyroid Cells of an Inositol Phosphateglycan, Putative Mediator of the cAMP-Independent Effects in the Gland." In Biology of Cellular Transducing Signals. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-0559-0_41.
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Gurnell, Mark, and V. Krishna Chatterjee. "Thyroid hormone resistance syndrome." In Oxford Textbook of Endocrinology and Diabetes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.3282.
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Thyroid hormones (thyroxine T4 and triiodothyronine T3) regulate many cellular processes in virtually every type of tissue. The diverse effects of thyroid hormone include regulation of growth, control of basal metabolic rate, enhanced myocardial contractility, and functional differentiation of the central nervous system. The synthesis of thyroid hormones is controlled by hypothalamic thyrotrophin-releasing hormone (TRH) and pituitary thyroid-stimulating hormone (TSH), and in turn, T4 and T3 regulate TRH and TSH production as part of a negative feedback loop.
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Visser, Theo J. "Biosynthesis, transport, metabolism, and actions of thyroid hormones." In Oxford Textbook of Endocrinology and Diabetes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.3010.
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In healthy humans with a normal iodine intake, the thyroid follicular cells produce predominantly the prohormone thyroxine (3,3′,5,5′-tetraiodothyronine; T<sub>4</sub>), which is converted in peripheral tissues to the bioactive hormone 3,3′,5-triiodothyronine (T<sub>3</sub>) or to the inactive metabolite 3,3′,5′-triiodothyronine (reverse T<sub>3</sub>). The bioavailability of thyroid hormone in target tissues depends to a large extent on the supply of plasma T<sub>4</sub> and T<sub>3</sub>, the activity of transporters mediating the cellular uptake and/or efflux of these hormones, as well as the activity of deiodinases and possibly other enzymes catalyzing their activation or inactivation. Thyroid function is regulated most importantly by the hypophyseal glycoprotein thyroid-stimulating hormone (TSH), also called thyrotropin. In turn, TSH secretion from the anterior pituitary is stimulated by the hypothalamic factor thyrotropin-releasing hormone (TRH). TSH secretion is down-regulated by negative feedback action of thyroid hormone on the hypothalamus and the pituitary. The contribution of locally produced T<sub>3</sub> versus uptake of plasma T<sub>3</sub> is much greater for some tissues such as the brain and the pituitary than for most other tissues. Plasma TSH is an important parameter for the diagnosis of thyroid dysfunction but is not representative for the thyroid state of all tissues. In this chapter various aspects will be discussed of: (a) the neuroendocrine regulation of thyroid function, (b) the biosynthesis of thyroid hormone (i.e. the prohormone T<sub>4</sub>), (c) the activation and inactivation of thyroid hormone in peripheral tissues, and (d) the mechanism by which T<sub>3</sub> exerts it biological activity. A schematic overview of the hypothalamus– pituitary–thyroid–periphery axis is presented in Fig. 3.1.2.1.
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Wittmann, Gabor, Judit Menyhert, Edith Sanchez, et al. "Evidence for GABA-Mediated Effects on TRH-Producing Neurons in the Hypothalamic Paraventricular Nucleus of TRH-GFP Mice." In BASIC - Hypothalamic-Pituitary-Thyroid Axis: Thyroid Hormone Metabolism, Cellular Uptake & Action. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p16.p1-651.
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Farid, Nadir R., Goverdina Fåhraeus-van Ree, and Rosario Briones-Urbina. "STRUCTURE, SYNTHESIS, CELLULAR LOCALIZATION AND IMMUNOGENICITY OF THE TSH RECEPTOR." In Autoimmunity and the Thyroid. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-12-731950-6.50020-6.
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Peltsverger, Maya Y., Peter W. Butler, Sheila M. Smith, et al. "The -258 A/G Type 2 Deiodinase Gene Polymorphism Is Associated with a Differential Response in the Pattern of Thyroid Hormone Secretion after TRH-Stimulated TSH Release." In BASIC - Hypothalamic-Pituitary-Thyroid Axis: Thyroid Hormone Metabolism, Cellular Uptake & Action. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p16.p1-655.
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Cho, Cho, Thinzar Aye, Aung Khaing, and Takaomi Kobayashi. "Comparative Study of Cellulose Hydrogel Films Prepared from Various Biomass Wastes." In Cellulose [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99215.
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The conversion of biomass waste products to valuable products like cellulose hydrogel films is important in cell regeneration. In this study, the various biomass wastes: thanaka heartwood (TH), sugarcane bagasse (SB) and rice straw (RS) were used as cellulose resources. They were chemically treated using acid and alkali to obtain cellulose fibers. The yield percent of cellulose fibers depends on the nature of biomass materials. Scanning Electron Microscope (SEM), X-ray Diffraction (XRD) and Fourier Transform Infrared Spectroscopy (FTIR) analyses showed that the amount of lignin and hemicellulose from these samples were successfully reduced by chemical treatment. Cellulose fibers were treated using the dimethylacetamide/lithium chloride (DMAc/LiCl) system to obtain cellulose hydrogel solutions. Following this, the cellulose hydrogel films were prepared employing the phase inversion method without cross-linker. These films were transparent and flexible. In the present study, water retainable property and viscoelasticity of cellulose hydrogel films were measured. Antimicrobial activity tests of cellulose solutions have been carried out to be utilized to hydrogel films for biomedical application.
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Demeneix, Barbara Anne, Stephanie Decherf, Isabelle Seugnet, and Marie Stephanie Clerget-Froidevaux. "RXR Isoforms Exert Differential Effects on T3-Dependent Repression of Trh Transcription." In BASIC - Hypothalamic-Pituitary-Thyroid Axis: Thyroid Hormone Metabolism, Cellular Uptake & Action. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p16.p1-650.
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Chiappini, Franck, Kristen R. Vella, Felix D. Ye, and Anthony N. Hollenberg. "Family Members CREB1 and CREM Control Thyrotropin-Releasing Hormone (TRH) Expression in the Hypothalamus." In BASIC - Hypothalamic-Pituitary-Thyroid Axis: Thyroid Hormone Metabolism, Cellular Uptake & Action. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p16.p1-649.
Full textConference papers on the topic "Cellule TFH"
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Kim, Jaehwan, Sang Yeol Yang, Min Hee Lee, et al. "Cellulose Smart Material for Sensor, Actuator and MEMS Applications." In ASME 2008 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. ASMEDC, 2008. http://dx.doi.org/10.1115/smasis2008-381.
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Cellulose Electro-Active Paper (EAPap) has been discovered as a smart material that can be used as a sensor and actuator [1]. It has many advantages in terms of low voltage operation, light weight, low power consumption, low cost, biocompatibility and biodegradability. EAPap is made with cellulose paper coated with thin electrodes. EAPap shows a reversible and reproducible bending movement as well as longitudinal displacement under electric field. The out-of-plane bending deformation is useful for achieving flapping wings, micro-insect robots, and smart wall papers. On the other hand, in-plane strains, such as extension and contraction of EAPap materials are also promising for artificial muscle applications. The actuation principle of cellulose EAPap bending actuator is known to be a combination of piezoelectric effect and ion migration effect. This paper presents further investigation of cellulose EAPap for actuator, sensor and MEMS devices. Piezoelectricity is one of major actuating mechanism of cellulose EAPap. Cellulose is a complex anisotropic material. Aligning cellulose fibers in the fabrication process is a critical parameter to improve mechanical and electromechanical properties of EAPap such as stiffness, strength, piezoelectricity and so on. Cotton cellulose fibers are dissolved into a solution using NaOH/urea and DMAc/LiCl methods. In the later method, the dissolution and shaping of cellulose can be carried out by DMAc/LiCl. Cellulose pulp was mixed with lithium chloride (LiCl) and dehydrated by heating. After adding DMAc (N, N-dimethylacetamide) to the mixture, swell it in room temperature. By heating it a solution formation can be obtained. There are some issues on eliminating solvent and ions and regenerating a pure cellulose films. The material processing all about EAPap has been introduced [2, 3]. Wet drawn stretching method is used in the fabrication process of cellulose film to increase its mechanical and electromechanical properties. This wet-drawn cellulose EAPap is termed as Piezo-Paper. Cellulose EAPap material can be customized to satisfy the material requirement for specific applications. Piezo-Paper can be used for strain sensors, vibration sensors, ultrasonic transducers, SAW devices, speakers, microphones, stack actuators, bending actuators and MEMS devices. Figure 1 shows some applications. Piezoelectric charge constant of Piezo-Paper is 70 pC/N. Details of piezoelectric characteristics of Piezo-Paper and its applications are presented in this paper. Micro-fabrication on cellulose EAPap has many applications, for example, MEMS sensors, e-Paper, thin film transistor (TFT), and even microwave-driven EAPap actuator. To develop microwave-driven EAPap actuator, rectenna (rectifying antenna) has been developed [4]. Rectenna can rectify microwaves and feed dc power without wire. Thus, this technology has many applications. To fabricate the rectenna array on cellulose EAPap, micro patterning of metallic layer and Schottky diode fabrication were studied. The Schottky diode fabrication gives the possibility of TFT on cellulose sheet. Advancing from this technology, SAW (Surface Acoustic Wave) device fabrication for humidity sensor is possible. The devices fabrication along with the characterization and their demonstration will be shown. Cellulose EAPap technology will bring the dream of flying magic paper into real world in the near future.
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Strano, Matteo. "Metal Foam Filled Hydroformed Tubes: Production and FEM Simulation." In ASME 2010 International Manufacturing Science and Engineering Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/msec2010-34210.
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The marriage of the Tube HydroForming (THF) process with metal foams is interesting for different reasons: a) THF parts are naturally suited as cases to be filled by an internal metallic foam reinforcement and therefore for structural applications; b) the possibility to increase the mechanical strength of hydroformed parts allows to plan the THF process more freely and flexibly. These components, made of an outer hollow thin compact metal skin and a cellular lightweight core may find several applications in different industrial fields. In order to allow for an efficient and effective product/process design with a concurrent engineering approach, the structural performance of these composite parts must be predicted by means of FEM calculation. The optimal combination of tube and metal foam properties must be found. While FEM simulation of bending and hydroforming is state of the art, the accurate FEM simulation of the mechanical behavior of metal foams cannot be considered fully established. In the first part of this paper the foam-filling production cycle of a simple hydroformed aluminum part is shown, in order to discuss some of the design and manufacturing issues that can be faced in FEM based product/process analysis, concerning the thermal effects on the tube materials, the ability of completely filling the tube, the foam/tube interface conditions, the uniformity of cell distribution. A few potential applications of foam-filled hydroformed tubes are also presented. In the second part of the paper, the common methods and formulations for FEM simulation of foam based structures are discussed, and a new and very promising method is proposed.
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Győri, István, and Ferenc Hartung. "Stability results for cellular neural networks with delays." In The 7'th Colloquium on the Qualitative Theory of Differential Equations. Bolyai Institute, SZTE, 2003. http://dx.doi.org/10.14232/ejqtde.2003.6.13.
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Morrissey, J. H., S. A. Gregory, and T. S. Edgington. "DIFFERENTIAL EXPRESSION AND SUBCELLULAR LOCALIZATION OF TISSUE FACTORIN A CONSTITUTIVE VERSUS AN INDUCIBLE CELL TYPE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643739.
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Tissue factor (TF) is an integral membraneglycoprotein and receptor present on a variety of cells outside of the vasculature, but normally absent from intravascular cells. TF plays a central role in initiation of coagulation by rapidly binding and allosterically activating bound factor Vll/VIIa, which proteoly-tically activates coagulation factors IX and X. This protease cascade appears to play a role in the cellular inflammatory response, during which endothelial cells and monocytes/macrophages can be induced to express cell surface TF.Monocyte TF can be induced in response to endotoxin and also via direct interaction with activated T cells and by a specific lymphokine.We have developed a panel of polyclonaland twenty-nine high affinity monoclonal antibodies to human TF. The antibodies recognize TF epitopes under a broad range of conditions, some of which rapidly and efficiently neutralize <95% of TF activity isolated from brain, placenta and expressed bycultured cells. Using these antibodies in immunohistochemical assays, we haveobserved little or no TF antigen cytologically associated with resting monocytes, noTF activity, and following stimulation, the cytologic appearance of TF antigen parallels the acquisition of TF activity.Immunohistochemical staining of stimulated monocytesis diffuse, consistent with homogeneous cell-surface distribution of the TF molecule.In addition, the normal human fibroblastic cell lines GM1380 and GM1381, whichexpress TF const itutively, show a cytologically different and much more intense pattern of intracellular inclusions of TF. This is consistent with previous observationsthat lysed cells show about five-fold moreTF activity than do intact cells. These findings indicate the presence of an intracellular storage site for TF in some cell types, a pattern presently associated only with constitutive expression of this receptor protein. In addition, they confirm thatTF is induced in stimulated monocytes rather than translocation or modification. Supported by NIH grants HL-16411 and CA-41085.
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Singh, Prabhjot, Mithilesh Kumar, and Ambarish Das. "Effective frequency planning to achieve improved KPI's, TCH and SDCCH drops for a real GSM cellular network." In 2014 International Conference on Signal Propagation and Computer Technology (ICSPCT). IEEE, 2014. http://dx.doi.org/10.1109/icspct.2014.6884924.
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Knoller, S., and N. Savion. "MODULATION OF ANTITHROMBIN III ACTIVITY AND ANTITHROMBIN III-THROMBIN COMPLEXES BINDING TO CULTURED CELLS BY MONOCLONAL ANTIBODIES AGAINST ANTITHROMBIN III." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644361.
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Two monoclonal antibodies (mAb's) against antithrombin III (ATIII) were characterized with respect to their ability to interfere with ATIII activity. AT III activity was measured by its ability to inhibit the amidolitic activity of thrombin on the substrate BCP-100. Incubation of 150 ng of ATIII with 28pg mAb A36R2 prior to addition of 50 ng thrombin totally abolishes the inhibitory effect of ATIII on thrombin. Incubation of 200ng of ATIII with 10 μg of mAb B26R4 prior to addition of 75 ng thrombin raises the inhibitory effects of ATIII from 37% to 100%. We examined the effect of these mAb's on binding of antithrombin III-thrombin (ATIII-Th) complexes to bovine corneal endothelial cells. 120 pg/ml mAb's are reacted with 2 μg/ml ATIII-Th complexes prior to their addition to the cells. mAb A36R2 completely blocks ATIII-Th complexes binding. In contrast, mAb B26R4 enhances binding up to 250% of the control binding.We conclude that mAb A36R2 prevents binding of thrombin to ATIII by recognizing an epitope on ATIII close to thrombin binding site or that its binding to ATIII induces a conformational change in the thrombin binding site thus it no longer recognizes thrombin. mAb B26R4 has a heparin-like effect on ATIII: Its binding to ATIII induces conformational changes which improve thrombin binding to ATIII. There is a correlation between inhibition and enhancement of thrombin binding to ATIII and of ATIII-Th complexes binding to cells by the two mAb's. These mAb's may provide a new tool to control the activity of ATIII and to identify the cellular binding site on the ATIII-Th complex.This research was supported by a grant from the National Council for Research and Development, Israel and G.S.F. München, Germany.
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Jaworski, Nazariy, Mykhaylo Lobur, and Marek Iwaniec. "Implementation features of cellular composites microlevel structural models construction based on Voronoi tessellation and OpenCL technology usage." In 2018 XIV-th International Conference on Perspective Technologies and Methods in MEMS Design (MEMSTECH). IEEE, 2018. http://dx.doi.org/10.1109/memstech.2018.8365713.
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Ji, Yali, Isaac Rodriguez, and Gary L. Bowlin. "Electrospinning of Chitin Whisker-Reinforced Nanocomposite Fibrous Scaffolds." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80104.
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Chitin is the second most abundant biopolymer next to cellulose and possesses many favorable properties such as non-toxicity, high crystallinity, biocompatibility and biodegradability. Acid-treatment of chitin can dissolve regions of low lateral order, resulting in elongated rod-like nanocrystals, termed “whiskers”. Chitin whiskers (CWs) are an emerging and novel nanofiller that have been shown to bring about reinforcing effects on both synthetic and natural polymeric structures. The biocompatibility and biodegradability also make it one of the most promising fillers.1 However; it was thought that CWs can only well disperse in aqueous solution, and poorly disperse in organic solvents, which to some extent restricts the development of CW-based nanocomposites. In a previous study, we found that the CW can be well dispersed in 1,1,1-trifluoroethanol (TFE) solvent which is a good solvent for commonly used biodegradable polymers such as polycaprolactone (PCL), polylactide (PLA) and polydioxanone (PDO). Thus, it is possible to blend CWs with these biopolymers to prepare nanocomposite scaffolds. Electrospinning is a rather simple and promising technique to fabricate scaffolds, since the resulting microstructures are similar to the extracellular matrix (ECM) with potential facilitate the design of surgical implants and promote tissue regeneration. Thus, the focus of this work was to develop CW-reinforced nanocomposite fiber scaffolds via electrospinning and investigate their mechanical and biological properties, expecting them to be potential candidates for bone tissue engineering applications.
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Falang, A., G. M. Alessio, M. Donati, and T. A. Barbui. "DISSEMINATED INTRAVASCULAR COAGULATION (DIC) AND ACUTE LEUKEMIA:IDENTIFICATION OF A NEW CELLULAR PROCOAGULANT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643661.
Full textAbstract:
There is an enhanced incidence (>50%) of severe coagulopathy in association with several types of acute leukemias. Cell associated procoagulants are considered important in this context. So far only a Tissue Factor (TF)-type procoagulant has been described in leukemic cells. We have set up here the experimentalconditions to identify other possible cellular procoagulants in leukemia. We have tested blast cell extracts from 21 patients with 5 different cytological subtypes (from Ml to M5 of acute non lymphoid leukemia (ANLL), according to theFAB classification, in order to assay whether they express "cancer procoagulant" (CP), a F VH-independent FX activating cysteine proteinase (Falanga … Gordon, 1985; Donati, et al. 1986). All the samples shortened the recalcification time of normal human plasma, the effect being significantly greater (p<0.001) in the M3 group. The activity was 20% to 100% independent from the presence of FVII and was susceptible to 2 cysteine proteinase inhibitors (Iodoacetamide, 2 mM, and HgCl2 ,0.1 mM) in all of the extracts but the M5 type. In addition, M2 and M3 samples directly activated pure FX in a two stage clotting assay. Control cell extracts from 10 healthy donors did not show any procoagulant activity, under the same conditions. This study provides evidence for a new procoagulant expressed by cells of ANLL; the peculiar characteristics of this procoagulant (i.e. its confinement to the malignant phenotype, its shedding into the plasma, its possible modulation by vitamin K antagonists) make this observation of potential interest in the development of new diagnostic and therapeutic tools in ANLL.
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Le Choismier, H. "Un transporteur d’oxygène universel d’origine marine au service de la santé." In 66ème Congrès de la SFCO. EDP Sciences, 2020. http://dx.doi.org/10.1051/sfco/20206601009.
Full textAbstract:
HEMARINA est une société de biotechnologie créée en 2007, qui développe un transporteur doxygène universel à partir de lhémoglobine M101 issue d’un annélide marin, Arenicola marina. Les caractéristiques de M101 sont déjà exploitées ou évaluées à des fins médicales par la société HEMARINA pour la préservation des organes dans les cas de transplantation (HEMO2life®, Thuillier et al, 2011, Teh et al, 2017 ; Mallet et al., 2014), en tant que pansement actif favorisant la cicatrisation et loxygénation de plaies hypoxiques (HEMHealing®, brevet international Ref. WO2009/007532, intitulé « Utilisation d’une hémoglobine pour la préparation de pansements, et pansements ainsi preparés »), comme transporteur doxygène universel en transfusion (HEMOXYCarrier®, Rousselot et al., 2006), et comme activateur de croissance cellulaire in vitro (HEMOXCell®/HEMUPStream®, Le Pape et al, 2015). Depuis 2018, HEMARINA a élargi son champ dapplication en souvrant au domaine dentaire. Les maladies parodontales en tant quinfections polymicrobiennes sont un danger pour la santé surtout chez les patients à risque. Elles sont impliquées dans la survenue ou laggravation des certaines situations pathologiques tels que les cardiopathies, les maladies respiratoires, le déséquilibre du diabète et les accouchements prématurés (Ide et al, 2011, Detert et al., 2010, Huck et al., 2011). Les parodontites sont un enjeu de santé publique et leur traitement vise non seulement à conserver les organes et implants dentaires fonctionnels, mais surtout à protéger lorganisme contre les pathologies générales associées (Fremont et al, 2008). HEMARINA développe HEMDental-Care, M101 formulé sous forme de gel, destiné à ê tre utilisé comme adjuvent aux traitements parodontaux pour ses propriétés antibactériennes. En plus d’un possible effet sur les dysbioses, M101 pourrait in vivo favoriser les processus de réparation des tissus (mous et durs) (HEMDental-Regenerativ). En effet, il a été démontré que lajout de M101 dans les milieux de culture favorise la croissance de lignées cellulaires in vitro (Le Pape et al., 2017 a) et favorise la recolonisation de greffons osseux allogéniques par les cellules souches mésenchymateuses ( Le Pape et al., 2017 b).
Reports on the topic "Cellule TFH"
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Eshed-Williams, Leor, and Daniel Zilberman. Genetic and cellular networks regulating cell fate at the shoot apical meristem. United States Department of Agriculture, 2014. http://dx.doi.org/10.32747/2014.7699862.bard.
Full textAbstract:
The shoot apical meristem establishes plant architecture by continuously producing new lateral organs such as leaves, axillary meristems and flowers throughout the plant life cycle. This unique capacity is achieved by a group of self-renewing pluripotent stem cells that give rise to founder cells, which can differentiate into multiple cell and tissue types in response to environmental and developmental cues. Cell fate specification at the shoot apical meristem is programmed primarily by transcription factors acting in a complex gene regulatory network. In this project we proposed to provide significant understanding of meristem maintenance and cell fate specification by studying four transcription factors acting at the meristem. Our original aim was to identify the direct target genes of WUS, STM, KNAT6 and CNA transcription factor in a genome wide scale and the manner by which they regulate their targets. Our goal was to integrate this data into a regulatory model of cell fate specification in the SAM and to identify key genes within the model for further study. We have generated transgenic plants carrying the four TF with two different tags and preformed chromatin Immunoprecipitation (ChIP) assay to identify the TF direct target genes. Due to unforeseen obstacles we have been delayed in achieving this aim but hope to accomplish it soon. Using the GR inducible system, genetic approach and transcriptome analysis [mRNA-seq] we provided a new look at meristem activity and its regulation of morphogenesis and phyllotaxy and propose a coherent framework for the role of many factors acting in meristem development and maintenance. We provided evidence for 3 different mechanisms for the regulation of WUS expression, DNA methylation, a second receptor pathway - the ERECTA receptor and the CNA TF that negatively regulates WUS expression in its own domain, the Organizing Center. We found that once the WUS expression level surpasses a certain threshold it alters cell identity at the periphery of the inflorescence meristem from floral meristem to carpel fate [FM]. When WUS expression highly elevated in the FM, the meristem turn into indeterminate. We showed that WUS activate cytokinine, inhibit auxin response and represses the genes required for root identity fate and that gradual increase in WUCHEL activity leads to gradual meristem enlargement that affect phyllotaxis. We also propose a model in which the direction of WUS domain expansion laterally or upward affects meristem structure differently. We preformed mRNA-seq on meristems with different size and structure followed by k-means clustering and identified groups of genes that are expressed in specific domains at the meristem. We will integrate this data with the ChIP-seq of the 4 TF to add another layer to the genetic network regulating meristem activity.