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Literatura académica sobre el tema "T-cell subpopulations"

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Publicado: 10 de marzo de 2023

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Artículos de revistas sobre el tema "T-cell subpopulations"

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Tian, Yamin, Seiichiro Kobayashi, Nobuhiro Ohno, Masamichi Isobe, Mayuko Tsuda, Yuji Zaike, Nobukazu Watanabe, Kenzaburo Tani, Arinobu Tojo y Kaoru Uchimaru. "Leukemic T Cells Are Specifically Enriched In a Unique CD3dimCD7low Subpopulation of CD4+ T Cells In Acute-Type Adult T Cell Leukemia". Blood 116, n.º 21 (19 de noviembre de 2010): 4144. http://dx.doi.org/10.1182/blood.v116.21.4144.4144.

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Abstract Abstract 4144 [Background] Adult T-cell leukemia (ATL) is a malignant disorder caused by human T-cell leukemia virus type I (HTLV-I). Morphological discrimination of leukemic cells from non-leukemic T cells is often difficult in ATL since ATL cells reveal morphological diversity except for typical “flower cells”. Although a study using CD3 gating in flow cytometry reported that ATL cells were distinguishable as a CD3low population from normal lymphocytes, these cells were not well characterised as ATL cells. Considering that defective expression of CD7 as well as CD3 is common in ATL cells, we applied multi-color flow cytometry to detect a putative leukemia-specific cell population in the peripheral blood from ATL patients. [Methods and Results] (1) In flow cytometry, after dead-cell and monocyte removal, CD4+ T lymphocytes were gated on the CD3 versus CD4 plot. Based on cell density and fluorescence intensity of CD3 and CD7 in this population, we designated three subpopulations on this plot: CD3highCD7high, CD3dimCD7dim and CD3dimCD7low(Results of a representative ATL and a control sample are shown in Figure). The proportion of the CD3dim/CD7low subpopulation was significantly higher in acute-type ATL CD4+ lymphocytes than in normal controls(Figure). (2) To extensively characterise this subpopulation, we next estimated the HTLV-I proviral load by quantitative real-time PCR after FACS sorting based on this CD3 versus CD7 plot. In all patient samples, HTLV-I proviral integration was detected in all subpopulations. However, the proviral load was significantly higher in the CD3dim/CD7low subpopulation compared to the CD3high/CD7high subpopulation. Almost all of the cells in the CD3dim/CD7low subpopulation were HTLV-I infected. (3) We next examined CCR4 and CD25 expression in each subpopulation. Both CCR4 and CD25 expression levels were maintained at very low and similar levels throughout all subpopulations in normal control cells and in the CD3high/CD7high subpopulation of patients with ATL as well. In contrast, CCR4 expression was significantly up-regulated in CD3dim/CD7low subpopulation of patients with ATL compared to the CD3high/CD7high subpopulation (MFI: 36.5±17.2 vs. 3.8±1.1). The expression of CD25 was also up-regulated in the subpopulation (MFI: 7.8±8.0 vs. 2.7±1.6). (4) Monoclonal expansion of HTLV-I-infected cells in the CD3dim/CD7low subpopulation was indicated by the genomic integration site analysis using a long inverse polymerase chain reaction (PCR) method. (5) We reviewed the glass-slide specimens of FACS-sorted samples to evaluate the morphology of each subpopulation on the CD3 versus CD7 plot. Atypical lymphocytes with morphology such as a notch in the nucleus were observed in all subpopulations. The majority of sorted cells from CD3dim/CD7low subpopulation showed “flower cell”-like morphology. (6) We also detected a small CD3dim/CD7dim subpopulation other than the CD3dim/CD7low and CD3high/CD7high subpopulations in all patients with acute-type ATL who were analysed(Figure). This subpopulation contained the same clone as the CD3dim/CD7low subpopulation, although a phenotypical difference existed between these subpopulations. [Conclusion] (1) Above findings indicate that leukemic T cells are specifically enriched in a unique CD3dim/CD7low subpopulation of CD4+ T cells in acute-type ATL. This multi-color FACS system may be useful for precisely monitoring disease during chemotherapy, detecting minimal residual disease and analysing ATL cells. (2) Previous reports have revealed that HTLV-I-infected cells transform through multi-step oncogenesis. Detailed analysis of these three subpopulations (CD3high/CD7high, CD3dim/CD7dim and CD3dim/CD7low) may give some insight into oncogenesis of HTLV-I-infected cells. Disclosures: No relevant conflicts of interest to declare.
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Phillips, S. M., D. Walker, S. K. Abdel-Hafez, G. P. Linette, B. L. Doughty, P. J. Perrin y N. el Fathelbab. "The immune response to Schistosoma mansoni infections in inbred rats. VI. Regulation by T cell subpopulations." Journal of Immunology 139, n.º 8 (15 de octubre de 1987): 2781–87. http://dx.doi.org/10.4049/jimmunol.139.8.2781.

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Abstract These studies assess the roles of subpopulations of T lymphocytes in inducing and modulating resistance to Schistosoma mansoni. CDF rats were depleted of RT 7.1+ (anti-Pan-T), W3/25+ (anti-T helper/inducer), or OX8+ (anti-T suppressor) cells by the in vivo administration of monoclonal antibodies (mAb). The development of parasites and immunity to challenge by S. mansoni were compared with results in undepleted normal and congenitally athymic rats. Discrete subpopulations of T lymphocytes were adoptively transferred to ascertain effects upon parasite development and the protective immune response. In vitro studies, involving utilizing cocultivation of cell subpopulations +/- cyclosporin A, were utilized to dissect mechanisms. Depletion of T lymphocytes by anti-RT7.1 mAb and anti-W3/25 mAb resulted in augmented initial worm development, suboptimal resistance, and decreased antibody and delayed-type hypersensitive reactivity directed against schistosome antigens. Depletion with OX8 mAb produced opposite effects. The adoptive transfer of T cell subpopulations produced concordant results with T cell regulation expressed B cell-dependent effector mechanisms. The coadoptive transfer of cells resulted in the suppression of resistance afforded by the W3/25+ cells by OX8+ cells, which could be augmented in vitro by cyclosporin A. Thus, protective immunity to S. mansoni in rats is regulated by discrete subpopulations of T lymphocytes. The findings suggest the possibility of selective immune regulation of resistance based on the manipulation of specific T cell subpopulation.
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Kanof, Marjorie E. "Purification of T Cell Subpopulations". Current Protocols in Immunology 00, n.º 1 (diciembre de 1991): 7.3.1–7.3.5. http://dx.doi.org/10.1002/0471142735.im0703s00.

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Kubick, Norwin, Patrick C. Henckell Flournoy, Ana-Maria Enciu, Gina Manda y Michel-Edwar Mickael. "Drugs Modulating CD4+ T Cells Blood–Brain Barrier Interaction in Alzheimer’s Disease". Pharmaceutics 12, n.º 9 (16 de septiembre de 2020): 880. http://dx.doi.org/10.3390/pharmaceutics12090880.

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The effect of Alzheimer’s disease (AD) medications on CD4+ T cells homing has not been thoroughly investigated. CD4+ T cells could both exacerbate and reduce AD symptoms based on their infiltrating subpopulations. Proinflammatory subpopulations such as Th1 and Th17 constitute a major source of proinflammatory cytokines that reduce endothelial integrity and stimulate astrocytes, resulting in the production of amyloid β. Anti-inflammatory subpopulations such as Th2 and Tregs reduce inflammation and regulate the function of Th1 and Th17. Recently, pathogenic Th17 has been shown to have a superior infiltrating capacity compared to other major CD4+ T cell subpopulations. Alzheimer’s drugs such as donepezil (Aricept), rivastigmine (Exelon), galantamine (Razadyne), and memantine (Namenda) are known to play an important part in regulating the mechanisms of the neurotransmitters. However, little is known about the effect of these drugs on CD4+ T cell subpopulations’ infiltration of the brain during AD. In this review, we focus on understanding the influence of AD drugs on CD4+ T cell subpopulation interactions with the BBB in AD. While current AD therapies improve endothelial integrity and reduce astrocytes activations, they vary according to their influence on various CD4+ T cell subpopulations. Donepezil reduces the numbers of Th1 but not Th2, Rivastigmine inhibits Th1 and Th17 but not Th2, and memantine reduces Th1 but not Treg. However, none of the current AD drugs is specifically designed to target the dysregulated balance in the Th17/Treg axis. Future drug design approaches should specifically consider inhibiting CD4+ Th17 to improve AD prognosis.
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Leonhardt, U., U. Wagner, M. Werner y L. Engelmann. "T-cell-subpopulations in septic patients". Critical Care 5, Suppl 1 (2001): P059. http://dx.doi.org/10.1186/cc1127.

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Ferrara, Andrea, Marvin M. McMillen y Garth H. Ballantyne. "T-cell subpopulations and colorectal cancer". Diseases of the Colon & Rectum 33, n.º 5 (mayo de 1990): 367–69. http://dx.doi.org/10.1007/bf02156259.

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Abramova, A. V., I. V. Galtseva, E. A. Mikhailova, N. M. Kapranov, Yu O. Davydova, Z. T. Fidarova, V. V. Troitskaya, E. N. Parovichnikova y V. G. Savchenko. "Oligoclonality and subpopulation structure of bone marrow T-cells in patients with aplastic anaemia". Russian journal of hematology and transfusiology 65, n.º 4 (10 de diciembre de 2020): 417–30. http://dx.doi.org/10.35754/0234-5730-2020-65-4-417-430.

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Introduction. The main pathogenetic mechanism of the development of aplastic anemia (AA) is a violation of the immune regulation of hematopoiesis.Aim: to study of the subpopulation composition of T-cells and the repertoire of the T-cell receptor in AA patients.Patients and Methods. The study included AA patients (n = 40) without prior immunosuppressive therapy in 2018–2020. The T-cell subpopulation structure and T-cell receptor Vβ-family (TCR-Vβ) oligoclonality were studied in samples of bone marrow using flow cytometry.Results. We report characteristic properties of T-cell subpopulations of bone marrow in all AA patients: elevated counts of cytotoxic T-cells, effector CD4+ and CD8+ cells, CD4+ memory cells, which may suggest a long-term antigenic stimulation with subsequent activation of these cell subpopulations resulting in hyperexpression of pro-inflammatory cytokines. Diminishing of naive CD4+ and CD8+ cells, regulatory and double negative T-cells may indicate a relaxing control of cytokine-producing T-cells. A relationship has been established between the AA severity and counts of effector, regulatory, double negative and PD-1 positive T-cells. A highest count of potentially cytokine-producing T-cells and lowest count of cells involved in T-cell activity regulation were observed in very severe AA patients. Studies of the TCR-Vβ repertoire revealed oligoclonal expansion in the cytotoxic T-cell subpopulation.Conclusion. Enrichment in selected Vβ families suggests autoreactive T-cell clonality and attests to the immune nature of AA. A dynamic TCR-Vβ repertoire assay may be recommended in the disease monitoring. Flow cytometry helps identify valuable biomarkers for T-cell clone monitoring in AA and a better assessment of the disease progression.
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Hafler, D. A., D. A. Fox, D. Benjamin y H. L. Weiner. "Antigen reactive memory T cells are defined by Ta1." Journal of Immunology 137, n.º 2 (15 de julio de 1986): 414–18. http://dx.doi.org/10.4049/jimmunol.137.2.414.

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Abstract Ta1 is a 105,000 dalton protein that is weakly expressed on a small fraction of resting human peripheral blood T cells but strongly expressed in vitro on T cell clones and a substantial proportion of activated T cells. Unlike receptors for growth factors such as IL 2, the Ta1 antigen is present on T cell lines and clones irrespective of cell cycle. The function of Ta1 was investigated after separation of T lymphocytes into Ta1-enriched and Ta1-depleted subpopulations that were obtained from normal human subjects. Although Ta1-enriched T cells constitute only 10 to 15% of the E rosette-positive lymphocyte population, most, if not all, of the anamnestic response to the recall antigens tetanus toxoid and mumps reside in the Ta1+ population. Both Ta1-enriched and -depleted cells responded equally well to the mitogen PHA. The autologous mixed lymphocyte response was also greater in the Ta1-enriched subpopulation but not to the degree seen with soluble antigen. Increased proliferation was not due simple to increased inducer cell function within the Ta1+ subpopulations because both Ta1- and Ta1+ cells induced similar amounts of Ig synthesis in the presence of PWM. Additionally, increasing numbers of Ta1- cells did not suppress the enhanced proliferative responses of Ta1+ cells, and thus Ta1- cells do not appear to be functioning as suppressor cells. The Ta1 antigen appears to be a marker for previously activated T cells in peripheral blood, and this subpopulation appears to include T memory cells.
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SKÖLD, RYTTER, IVARS y CARDELL. "Characterization of Subpopulations of T-Cell Receptor Intermediate (TCRint) T Cells". Scandinavian Journal of Immunology 49, n.º 6 (junio de 1999): 611–19. http://dx.doi.org/10.1046/j.1365-3083.1999.00535.x.

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Bertrand, F. E., L. G. Billips, G. L. Gartland, H. Kubagawa y H. W. Schroeder. "The J chain gene is transcribed during B and T lymphopoiesis in humans." Journal of Immunology 156, n.º 11 (1 de junio de 1996): 4240–44. http://dx.doi.org/10.4049/jimmunol.156.11.4240.

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Abstract In mice and chickens, J chain appears to be expressed only in activated B cells and plasma cells. In humans, studies based mainly on transformed cells suggest that J chain expression may initiate during earlier stages in B lineage differentiation. In the present study, we isolated a series of hematopoietic subpopulations from human fetal and adult tissues by immunofluorescence cell sorting and examined each subpopulation for J chain expression by reverse transcriptase-PCR. In fetal and adult bone marrow, J chain transcripts were detected at all stages of B lineage differentiation, including the progenitor (CD34+/CD19-) and pro-B (CD34+/CD19+) cell subpopulations. J chain mRNA was also detected during fetal thymocyte development: double negative (CD4-/CD8-) through single positive (CD4+ or CD8+) cell subpopulations. The J chain message was not detected in peripheral CD3+ T cells, CD14+ monocytes, and CD56+ NK cells from either fetal or adult samples. The nucleotide sequence of J chain PCR products from CD34+/CD19- bone marrow progenitors and CD4+/CD8- thymocytes proved identical to the previously reported sequence of functionally spliced J chain mRNA. These results suggest that the J chain gene is transcriptionally active during early stages of both B cell and T cell differentiation, before the expression of their respective Ag receptors.
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Tesis sobre el tema "T-cell subpopulations"

1

McKnight, Andrew John. "The repertoire of lymphokine production by T cell subpopulations". Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.291402.

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Tormey, Vincent Joseph. "Regulation of macrophage subpopulations and their relationship to T-cell function in the pathogenesis of asthma". Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367893.

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Rogers, Paul R. "Analysis of CD45 Alternative Exon Expression in Murine and Human CD4+ T Cell Subpopulations: a Thesis". eScholarship@UMMS, 1993. http://escholarship.umassmed.edu/gsbs_diss/282.

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Leukocytes express a family of high molecular weight glycoproteins called leukocyte common antigens (CD45) which have tyrosine phosphatase activity and are involved in phosphotyrosine signal transduction. Antibodies to different CD45 isoforms distinguish functionally different CD4+ T cell subsets in humans, rats, and mice. Selected protein isoforms are expressed through a process of exon splicing which is cell-type and differentiation-state specific. Splicing of the three variable exons, A, B, and C, which encode amino acids located near the extracellular amino terminus of the protein, potentially results in generation of eight different mRNA transcripts. The purpose of this study was to determine the relative levels of all eight different CD45 transcripts present in a panel of murine CD4+ T cell lines and normal murine and human CD4+ T cell subsets separated with antibodies to CD45 variable exons. I show, as expected, that the broad features of CD45 surface isoform expression in these cells can be accounted for by the relative amounts of the eight differentially spliced transcripts. Unexpectedly, all the differences in CD45 isoform expression among the CD4+ T cell subpopulations that I measured could be accounted for by differences in the overall level of variable exon expression. I did not see differences among T cell populations in the relative expression of particular variable exons. Exon B was always found in greater abundance than exons C or A. Of the dual exon species, only AB and BC were found in CD4+ T cells. The AC species was undetectable. Human CD4+ T cells, especially those in the naive subset, express higher levels of CD45 variable exons than murine CD4+ T cells. In unrelated studies, I have generated a rat-mouse hybridoma which secretes a rat IgG antibody reactive with mouse CD45. I show that the monoclonal antibody, 25D10, defines a novel epitope consistent with a post-translational modification of CD45, similar but distinct from the epitope recognized by monoclonal antibody RA3.6B2 (anti-B220). This conclusion is based on evidence that it precipitates similar molecular weight bands from cells as does a framework monoclonal antibody to CD45, yet has a distinct cell surface expression as determined by flow cytometric analysis. It stains activated Th cell lines at a higher intensity than resting Th cells, stains 60-70% of splenocytes, and 25-30% of lymph node cells. It stains all class II positive cells but not freshly isolated CD4+, CD8+ T cells or CD45 transfected fibroblasts.
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4

Rädler, Diana [Verfasser] y Thomas [Akademischer Betreuer] Illig. "Mechanisms of immune regulation during development of atopic diseases in childhood : analysis of T cell subpopulations considering genetic and epigenetic influences / Diana Rädler. Betreuer: Thomas Illig". München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/104915312X/34.

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Jiang, Janina Q. "The production of HIV suppressive factors by CD28, CD38 and HLA-DR subpopulations of CD8+ T cells". Thesis, University of Ottawa (Canada), 2001. http://hdl.handle.net/10393/9104.

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We have examined CD8+ sub-populations to determine whether these subsets are critical to the production of CD8+ T cell nonlytic factors. The production of the beta-chemokines MIP-1alpha, MIP-1beta and RANTES, and the chemoattractant cytokine IL-16 were measured in cells derived from 24 HIV-infected and 25 uninfected subjects. Asymptomatic HIV+ subjects (CD4 > 200/ul) produced significantly higher levels of MIP-1alpha and MIP-1beta from CD8+ T cells and some sub-phenotypes. Higher RANTES levels were produced by CD28-, CD38- and HLA-DR+/- sub-phenotypes. However, IL-16 was only modulated in the CD38+ subset in comparison to total CD8+ T cells. Infection of CD8+ T cells and sub-populations resulted in generally increased levels of chemokine and IL-16 production, which dissipated over a 15 day time course. Moreover, CD8+ antiviral factor (CAF) activity, another major component of CD8+ T cell nonlytic suppression factors, was not associated with chemokine production. However, significantly higher levels of CAF were produced by CD38+ and HLA-DR+ sub-populations. In addition, we also showed that in CD8+ T cell populations, the production of MIP-1alpha, MIP-1beta and IL-16 was inversely correlated with virus copy number. These findings shed light on the noncytotoxic responses of CD8+ T cells in controlling the natural course of HIV infection.
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Mourah, Fadila. "Caractérisation phénotypique et fonctionnelle des sous-populations de monocytes dans les réponses immunitaires". Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC319/document.

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Les monocytes sont des leucocytes circulants dont la caractérisation est longtemps restée difficile. La dissection de l’ensemble de ces cellules en sous-populations fonctionnelles chez l’homme reste à ce jour insuffisante. Les monocytes sont cependant des précurseurs circulants de plusieurs populations de cellules dendritiques et de macrophages tissulaires, et occupent donc à ce titre une place prépondérante dans la mise en place des réponses immunitaires normales et pathologiques.À l'heure actuelle, trois sous-populations sont décrites chez l’homme : les monocytes classiques CD14+CD16neg, les non-classiques CD14dimCD16+ et les intermédiaires CD14+CD16+. Fonctionnellement, ces sous-populations sont diverses et hétérogènes et dotées de propriétés pro- et anti-inflammatoires apparemment redondantes. En pathologie, une augmentation du ratio entre CD16+ et CD16neg monocytes a été décrite en situation inflammatoire, suggérant un rôle des premières dans le développement et/ou l’amplification de l’inflammation. Parmi les monocytes non-classiques, des cellules capables de détecter des altérations de l’endothélium et ayant donc des propriétés spécifiques de surveillance du lit vasculaire ont été identifiées et caractérisées. Dans le but d’obtenir une meilleure définition des populations monocytaires et de les subdiviser en sous-populations où l’identification des fonctions de ces cellules serait plus accessible, je me suis attachée, dans ce travail de thèse, à analyser les différentes populations de monocytes humains circulants de manière aussi exhaustive que possible et avec les outils d’analyse biologiques et informatiques actuels. Les résultats, obtenus par l’analyse en cytométrie de flux de PBMC de 28 donneurs sains après marquage des cellules par vingt anticorps dirigés contre les molécules de surface, ont révélé l’existence d’une population de monocytes de plus grande taille. Ces « large » monocytes se subdivisent également en populations CD16neg et CD16+ (monocytes la14+16neg et la14+16+). Les monocytes restant ou « small » se composent de sm14+16neg largement majoritaires, de sm14+16+, et de sm14dim16+ auxquels se rajoutent des monocytes sm14lo16neg dont nous confirmons l’existence. L’expression des divers marqueurs sélectionnés a été faite par des méthodes d’analyse classiques, manuelles, ainsi que par l’utilisation d’algorithmes d’analyse non-supervisée. Les résultats ont montré les particularités d’expression propres à chaque population mais ont aussi indiqué que l’hétérogénéité phénotypique à l’intérieur de ces six populations de monocytes reste importante. Cependant, des profils d’expression qui sont partagés par plusieurs donneurs sains ont été identifiés. L’expression des molécules d’adhésion telles que CD49d, CD62L, CD162, ainsi que CD43 a été particulièrement utile pour cette identification. Quatre groupes phénotypiques majeurs ont ainsi été définis chez les 28 donneurs sains analysés
Monocytes are circulating leukocytes which characterization has long been difficult. Dissection of these cells into functional subpopulations in humans is still insufficient. Monocytes are however circulating precursors of several populations of dendritic cells and tissue macrophages, and play a prominent role in the development of immune response in steady state and pathology. At present, three monocyte subpopulations are described in humans: classical CD14+CD16neg, non-classical CD14dimCD16+ and intermediates CD14++CD16. Functionally, these subpopulations are diverse and heterogeneous and with apparently redundant pro - and anti-inflammatory properties. In pathology, an increase in the ratio of CD16 + to CD16neg monocytes has been described in inflammatory situation, suggesting a role of the former in the development and amplification of inflammation. Among the non-classical monocytes, cells that can detect changes in the endothelium and having then specific properties of vascular bed monitoring have been identified and characterized. In order to get a better definition of monocyte populations and break them down into subpopulations in which the identification of the cell functions would be more accessible, I endeavoured in this thesis work to analyse different populations of circulating human monocytes as comprehensively as possible and with state of the art analytical and computer tools. The results of flow cytometry analysis of PBMC from 28 healthy donors after cell staining with twenty antibodies directed against surface molecules revealed the existence of a population of monocytes of larger size
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7

Cohen, Shannon. "Identification et caractérisation fonctionnelle de sous-populations monocytaires circulantes chez l'homme". Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC241.

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Les monocytes sont des leucocytes circulants, précurseurs de cellules dendritiques et de macrophages, dont le phénotype est hétérogène. L’association entre les sous-populations de monocytes humains décrites dans la littérature et les fonctions dans la réponse immunitaire reste difficile. Les différentes populations de monocytes humains sont classées en fonction de l’expression de molécules de surface CD14 et CD16. Trois populations ont ainsi été identifiées : les monocytes classiques CD14+ CD16neg, les monocytes non-classiques CD14dim CD16+ et les monocytes intermédiaires CD14+ CD16+. Les fonctions attribuées à ces populations sont diverses et enchevêtrées. En particulier, les propriétés pro- et anti-inflammatoires associées à ces populations de cellules sont redondantes et conflictuelles suivant les auteurs. En situation inflammatoire, l’augmentation de la fraction de monocytes CD16+ suggère leur implication dans le développement et/ou dans l’amplification de l’inflammation. L’objectif de cette thèse porte sur une meilleure définition des populations monocytaires afin de pouvoir les subdiviser en sous-populations dont les fonctions seraient mieux définies. Ce travail s’est inscrit dans un projet à long terme du laboratoire visant à l’analyse phénotypique aussi exhaustive que possible des monocytes, utilisant les outils d’analyses biologiques et informatiques actuels. Cela a permis de mettre en évidence l’existence d’une population de monocytes de plus grande taille. Ces « large » monocytes se subdivisent en populations CD16neg et CD16+ (respectivement nommées la14+16neg et la14+16+). Les monocytes communément analysés, de taille plus petite ou « small », se subdivisent comme attendu en trois sous-populations identifiées ici comme monocytes sm14+16neg largement majoritaire, sm14dim16+ et sm14+16+....Enfin, l’analyse des phénotypes de monocytes circulants en situation pathologique a été effectuée chez des grands brûlés. Ces patients ont une susceptibilité accrue à l’infection due, entre autres, à des réponses immunitaires innées déficientes. Les résultats obtenus chez 18 patients prélevés à l’admission et à 7 et 28 jours plus tard permettent d’identifier différents profils de modifications phénotypiques des monocytes et leur évolution en fonction de l’état clinique. Cette étude a également permis de mettre en évidence l’existence d’une population de cellules à forte granulosité, amplifiée de façon importante chez les patients et dont les fonctions sont en cours d’analyse
Monocytes are circulating leucocytes, precursors of dendritic cells and macrophages, whose phenotype is heterogeneous. The association between human monocyte subsets described in the literature and the functions in the immune response remains difficult.The different populations of human monocytes are classified according to the expression of surface markers CD14 and CD16. Three populations have thus been identified: the classical monocytes CD14+ CD16neg, the non-classical monocytes CD14dim CD16+ and the intermediate monocytes CD14+ CD16+. The functions assigned to these populations are diverse and entangled. In particular, the pro- and anti-inflammatory properties associated with these populations are redundant and conflicting depending on the authors. In an inflammatory situation, the increase of the CD16+ monocyte fraction suggests their involvement in the development and/or the amplification of inflammation.The aim of this thesis is to improve the definition of monocytes populations so that they can be subdivided into subpopulations whose functions are better defined. This work was part of a long term laboratory project which has the goal to the most comprehensive phenotypic analysis of monocytes, using current biological and computer analysis tools. This highlighted to demonstrate the existence of a larger monocyte population. These "large" monocytes are subdivided into CD16neg and CD16+ populations (respectively named la14+16neg and la14+16+). Monocytes commonly analyzed, of smaller size or "small", are subdivided as expected in three subpopulations identified here as monocytes sm14+16neg largely in the majority, sm14dim16+ and sm14+16+.Finally, the analysis of the phenotypes of circulating monocytes in pathological situation was conducted in burn victims. These patients have an increased susceptibility to infection due, among other things, to deficient innate immune responses. These results obtained in 18 patients taken at admission and at 7 and 28 days later permitted to identify different phenotypic modification profiles of monocytes and their evolution depending on the clinical state. This study has also highlighted the existence of a population of cells with high granulosity, greatly amplified in patients and whose functions are being analyzed
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Blanc, Charlotte. "Lymphocytes T résidents mémoires dans les tumeurs du poumon et ORL : sous-populations et mécanismes de migration Cxcr6-deficiency impairs cancer vaccine efficacy and resident memory CD8+ T cells recruitment in tumor Phénotype et localisation des sous-populations de LT résidents mémoires dans les tumeurs pulmonaires". Thesis, Sorbonne Paris Cité, 2019. http://www.theses.fr/2019USPCB046.

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De grands bouleversements sont apparus au début du 21ème siècle dans la compréhension de la physiopathologie du cancer avec l'énoncé de la théorie de l'immunoédition complétant le concept de l'immunosurveillance. La communauté scientifique s'accorde désormais sur le fait que le système immunitaire et particulièrement les lymphocytes T (LT) CD8+ tiennent une place essentielle dans le contrôle de la croissance tumorale. Toutefois, par pression de sélection, la cellule tumorale développe des mécanismes de résistance aux attaques du système immunitaire, neutralisant ainsi l'effet cytotoxique des LT. Restaurer leurs fonctions antitumorales est une stratégie thérapeutique qui a fait ses preuves avec l'immunothérapie. Cependant, ces traitements ne sont pas toujours efficaces et peuvent être optimisés par une meilleure compréhension de l'immunité antitumorale. Dans ce but, nous nous sommes intéressés au déroulement de la réponse antitumorale des LT CD8+ en nous attardant sur les LT résidents mémoires (Trm) particulièrement efficaces contre la tumeur et au fort impact pronostic, qui pourrait être une cible thérapeutique pertinente. L'induction d'une réponse antitumorale efficace requière une présentation antigénique optimale conduisant à l'activation du LT CD8+ et à sa migration dans la tumeur via le réseau chimiokine/récepteur. Dans le premier travail, le récepteur de chimiokine CXCR6 a été identifié comme molécule de homing fortement exprimée par les LT CD8+ Trm du poumon. Sa chimiokine CXCL16 peut être sécrétée par les cellules présentatrices d'antigènes, les cellules épithéliales et tumorales mais le rôle de l'axe CXCR6/CXCL16 dans l'immunosurveillance des cancers n'est pas connu à ce jour. Pour en comprendre les mécanismes, des expériences de vaccinations antitumorales par voie intranasale (i.n.) réalisées dans des modèles de souris déficientes en CXCR6 ont permis de mettre en évidence l'impact de CXCR6 dans l'établissement d'une infiltration optimale en LT CD8+ spécifiques et Trm dans le lavage broncho-alvéolaire et au sein des tumeurs des voies aérodigestives supérieures. L'axe CXCR6/CXCL16 pourrait représenter un outil thérapeutique intéressant pour les vaccins anticancéreux ou pour les thérapies de transferts adoptifs de LT modifiés dont l'infiltration intra-tumorale est limitée. Les Trm ont la particularité d'exprimer des intégrines (CD103, CD49a) impliquées dans leur interaction avec le microenvironnement tumoral. Ils présentent un phénotype original microenvironnement-dépendant qui leur confère des avantages en termes d'activités cytotoxiques dans les tumeurs et expliquant leur impact pronostic favorable. Une meilleure connaissance de leur phénotype et de leurs mécanismes d'induction permettrait d'optimiser la réponse antitumorale. Le travail 2 s'est concentré sur l'étude de deux intégrines principales CD103 et CD49a dans les cancers pulmonaires par des techniques multiparamétriques d'immunofluorescence in situ et de cytométrie en flux. Les résultats montrent que leur expression expliquait l'infiltration des LT CD8+ et leur contact avec la cellule tumorale, en lien avec leur forte implication dans la survie des malades. Nos données suggérèrent également la possibilité d'un priming local pulmonaire nécessaire à l'induction du phénotype Trm par des modèles de vaccinations i.n. et d'un lien entre les structures lymphoïdes tertiaires et les Trm. Ces travaux ont montré l'importance de l'analyse de l'immunité locale avec les LT CD8+ Trm pour la compréhension de cette réponse antitumorale. Etudier le phénotype Trm a permis de mettre en lumière leur rôle crucial et leur potentiel comme cible thérapeutique. Une meilleure connaissance des mécanismes sous-jacents à l'induction des Trm permettra à terme de les cibler pharmacologiquement pour optimiser les thérapies et donc la survie des malades
With the immunoediting theory, new concept in the cancer physiopathology has appeared in the beginning of the 21st century. It is now established that the immune system and CD8+ T cells play a crucial role in tumor growth control. However, by selective pressure, the tumor cell develops mechanisms to avoid immune destruction and to inhibit T cells cytotoxicity. Reinvigorating antitumor functions is a well-proven therapeutic strategy with immunotherapy. Nevertheless, patients do not always respond to these treatments which could be optimized. In this context, we had studied antitumor response induction by focusing on CD8+ T cells and especially on resident memory T cells (Trm), new cytotoxic cells correlated with a good prognosis and which could be a relevant therapeutic target. A potent antitumor response requires an optimal antigenic presentation to prime CD8+ T cells and favor their migration into the tumor through chemokine network. In a first study, we identified a chemokine receptor CXCR6, highly expressed by lung CD8+ Trm. Its chemokine CXCL16 is produced by antigen presenting cells, epithelial and tumor cells, but the role of the CXCR6/CXCL16 axis in cancer immunosurveillance is not known yet. To understand its mechanisms, antitumor vaccinations strategies by intranasal (i.n.) route had been set up in CXCR6-deficient mice and had shown the role of CXCR6 in promoting the infiltration of specific CD8+ T cells and Trm in lung tissue and head and neck tumors. The CXCR6/CXCL16 axis could represent an interesting therapeutic tool for antitumor vaccines or adoptive cell transfer in which tumor infiltration is a challenge. Trm have the particularity to express integrins (CD103, CD49a) involved in the interaction with the tumor microenvironment. They exhibit an original and an heterogenous phenotype, microenvironment-dependent. Their phenotype is involved in their cytotoxic activities, highlighting their high prognostic impact and their potential to be a suitable therapeutic target. Better understanding Trm phenotype complexity and their induction mechanisms are crucial to further optimize antitumor response. The second work of this thesis focused on the expression of two main integrins CD103 and CD49a in lung cancer by an in situ multiparametric immunofluorescence technique and by flow cytometry. The results showed that their expression determine their contact with the tumor cells and their involvement in patient survival. Our data obtained by i.n. vaccination models and by tertiary lymphoid structures analysis suggest the possibility of a priming in the lung to induce the Trm phenotype. Our work shows the necessity of analyzing local immunity and CD8+ Trm T cells for a better understanding of antitumor response. Studying Trm phenotype has highlighted their crucial role and their potential to be a relevant therapeutic target. Identifying and targeting their mechanisms of induction might optimize therapies and patient's survival
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Qian, Chongsheng. "Immunothérapie adoptive pour le traitement des infections à Adénovirus réfractaires après allogreffes de Cellules Souches Hématopoïétiques : de la recherche fondamentale à la recherche clinique". Thesis, Université de Lorraine, 2017. http://www.theses.fr/2017LORR0069/document.

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L’allogreffe de cellules souches hématopoïétiques (CSH) est un des seuls traitements curatifs des hémopathies bénignes ou malignes et des déficits immunitaires primitifs. Cependant, les infections notamment virales ainsi que la réaction du greffon contre l’hôte comptent parmi les complications les plus fréquentes des allogreffes associées à une morbidité et une mortalité élevées. Les infections virales surviennent souvent en l’absence de reconstitution immunitaire spécifique dans un contexte d’immunosuppression liée à la GVHD elle-même ou à la prophylaxie ou au traitement de la GVHD. Les traitements médicamenteux anti-viraux préconisés présentent une efficacité inconstante dans ce contexte d’immunodéficience et ne sont pas dénués de toxicité. L’alternative thérapeutique prometteuse est l’immunothérapie adoptive cellulaire notamment celle qui consiste en l’injection de lymphocytes T spécifiques anti-viraux isolés par technique immunomagnétique (VSTs). Cependant, ces lymphocytes T peuvent être la cible des traitements immunosuppresseurs administrés pour la GVHD mais également par eux-mêmes être potentiellement la cause de la survenue ou de la réactivation d’une GVHD. Nous avons montré dans ce travail que l’efficacité des VSTs, qui repose sur leur expansion in vivo lors de la rencontre avec le virus circulant, est principalement permise par les sous-populations lymphocytaires les plus immatures, même si elles ne sont présentes qu’en faible proportion. Nous défendons dans ce travail le fait que l’efficacité des VST ainsi que leur persistance repose prioritairement sur la présence des sous-populations lymphocytaires T les plus immatures et ce quel que soit le degré de compatibilité HLA entre les VSTs et le receveur. De plus, leur sensibilité modérée aux corticoïdes, que nous avons étudiée in vitro, ne justifie pas la modulation de l’immunosuppression lors de l’injection des ADV-VSTs, comme observé in vivo dans le protocole clinique multicentrique de phase I/II que nous avons mené entre 2012 et 2015. En effet, ce protocole clinique ne rapporte aucune GVHD de novo après injection d’ADV-VSTs ; en revanche, la modulation de l’immunosuppression peut potentiellement être incriminée dans la réactivation de GVHD dans les semaines suivant l’injection des ADV-VSTs. La réalisation d’un essai comparatif de phase II permettra de prouver très clairement le rôle des VSTs dans la réactivation de GVHD
Hematopoietic stem cell transplantation (HSCT) is one of the only curative treatments for benign or malignant hematological diseases and primary immune deficiencies. However, viral infections and graft-versus-host disease (GVHD) are among the most frequent complications after HSCT associated with high morbidity and mortality. Viral infections often occur in the absence of specific immune reconstitution in the context of immunosuppression related to GVHD itself or to the prophylaxis or treatment of GVHD. The recommended anti-viral drug treatments have an inconsistent efficacy in this context of immunodeficiency and are not devoid of toxicity. The promising therapeutic alternative is adoptive immunotherapy, in particular the infusion of specific anti-viral T lymphocytes isolated by immunomagnetic technique (VSTs). However, these T lymphocytes may be targeted by immunosuppressive treatments administered for GVHD, but also may be the cause of the onset or reactivation of GVHD. We have shown in this work that the efficacy of VSTs, which is based on their in vivo expansion when they encounter the circulating virus, is mainly allowed by the most immature lymphocyte subpopulations, even in a small proportion. We argue in this work that the efficacy of VSTs and their persistence is mainly based on the presence of the most immature T lymphocyte subpopulations and this regardless of the degree of HLA compatibility between the VSTs and the recipient. Moreover, their moderate sensitivity to corticosteroids, which we have studied in vitro, does not justify the modulation of immunosuppression at the time of infusion of ADV-VSTs, as observed in vivo in the multicenter phase I / II clinical trial we conducted between 2012 and 2015. Indeed, this clinical trial does not report any de novo GVHD after ADV-VSTs infusion. On the other hand, modulation of immunosuppression may potentially be incriminated in the reactivation of GVHD within weeks of ADV-VST infusion. A Phase II comparative trial will bring the evidence of efficacy and will clearly determine the role of VSTs in the reactivation of GVHD
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Cohen-Kaminsky, Sylvia. "Analyse de composants cellulaires et moleculaires du microenvironnement thymique chez l'homme : interet dans l'etude du role du thymus dans la myasthenie". Paris 6, 1988. http://www.theses.fr/1988PA066157.

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Libros sobre el tema "T-cell subpopulations"

1

Ian, Kimber y Selgrade MaryJane K, eds. T lymphocyte subpopulations in immunotoxicology. Chichester: John Wiley & Sons, 1998.

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T-helper cell subpopulations. Copenhagen: Munksgaard, 1991.

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Kimber, Ian y MaryJane K. Selgrade. T Lymphocytes Subpopulations in Immunotoxicology. Wiley & Sons, Incorporated, John, 2007.

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Kisor, Robin L. A quantitative and functional analysis of T Lymphocyte subpopulations in protein and/or zinc deficient mice. 1988.

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Capítulos de libros sobre el tema "T-cell subpopulations"

1

Romagnani, Sergio. "T Cell Subpopulations". En History of Allergy, 155–64. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000358622.

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Ohigashi, Izumi y Yousuke Takahama. "Flow Cytometry Analysis of Thymic Epithelial Cells and Their Subpopulations". En T-Cell Development, 65–73. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2809-5_5.

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Katz, J., J. H. Eldridge y S. M. Michalek. "Rat T cell subpopulations: Effect of environmental and microbial antigens". En Advances in Mucosal Immunology, 186–87. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1848-1_53.

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Clement, Loran T., Max D. Cooper y Thomas F. Tedder. "Analysis of the Ontogeny and Function of Human Helper T Cell Subpopulations". En Leukocyte Typing II, 101–9. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4613-8587-5_8.

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Calvano, S. E., J. D. Albert, A. Legaspi, B. Organ, K. J. Tracey, S. F. Lowry, G. T. Shires y A. C. Antonacci. "T Cell Subpopulations Following Thermal Injury Effect of the Acute Stress Response". En Lipid Mediators in the Immunology of Shock, 349–60. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-0919-2_38.

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Bottomly, K., M. Luqman, J. Murray, J. West, A. Woods y S. Carding. "Clonal Expansion and Differentiation to Effector Function in Normal CD4 T Cell Subpopulations". En Progress in Immunology, 593–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83755-5_80.

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Minskaia, Ekaterina y João F. Lacerda. "Analysis of FOXP3 DNA Methylation Patterns to Identify Functional FOXP3+ T-Cell Subpopulations". En Methods in Molecular Biology, 115–36. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2647-4_9.

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Barrett, Douglas J., Desmond A. Schatz y John W. Sleasman. "Immunoregulatory CD4+ T Cell Subpopulations: Enumeration, Activation, and Functional Analyses in Normals and Autoimmune Disease". En Topics in Pediatrics, 83–95. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3230-8_8.

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Kronin, Vadim, Gabriele Süss, Ken Winkel y Ken Shortman. "The Regulation of T Cell Responses by a Subpopulation of CD8+DEC205+ Murine Dendritic Cells". En Advances in Experimental Medicine and Biology, 239–48. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4757-9966-8_40.

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Mami-Choubaid, F. y T. Hercend. "TCT.1: A Target Structure for a Subpopulation of Human γ/δ T Lymphocytes". En Function and Specificity of γ/δ T Cells, 189–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76492-9_26.

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Actas de conferencias sobre el tema "T-cell subpopulations"

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Nakstad, Britt y Torstein Lyberg. "PR0C0AGULANT ACTIVITIES IN HUMAN ALVEOLAR MACROPHAGES:". En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643159.

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The coexistence of fibrin and tissue macrophages is a common finding in the histopathology of chronic inflammatory diseases of the lung.Fibrin deposition may occur as a result of activation of the extrinsic coagulation system,initiated by procoagulants generated by alveolar macrophages.In this study human alveolar macrophages (LAM) obtained by lavage of healthy donors were shown to express procoagulant factors,thromboplastin (tissue factor) and a direct factor X activator,probably a thromboplastin/ factor VII complex.In contrast to blood monocytes, LAM were only slightly susceptible for in vitro induction of thromboplastin activity (11,3 ± 2,6 (SEM)-fold and 1,3 t 0,2-fold activity increase after endotoxin stimulation).LAM were separated into four subpopulations by density gradient centrifugation.The specific thromboplastin activity of subpopulation cells varied inversely with their density (3,08 ± 0,42 U/mg cell protein for the least dense vs.0.49 ± 0.03 for the most dense subpopulation ).Low-density subpopulations of LAM released membrane material to the culture medium,which was sedimentable in the u1tracentrifuge and which expressed procoagulant activities with the same characteristics as the LAM procoagu1 ants.These findings suggest that alveolar macrophages and the membrane vesicles shed from their surface can contribute to local fibrin deposition in the lungs by expressing procoagulant factors.
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Chen, Gregory M., Changya Chen, Rajat K. Das, Yang-Yang Ding, Bing He, Hannah Kim, David M. Barrett y Kai Tan. "Abstract PR3: Development of a transcriptomic T-cell atlas highlights the differential role of T-cell subpopulations in CAR T-cell therapy resistance". En Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-pr3.

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Pinho, Mariana Pereira y José Alexandre Marzagão Barbuto. "Abstract B069: Systemic alterations in T cell subpopulations of breast cancer patients". En Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b069.

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Di Sante, G., M. C. Caparello, B. Tolusso, C. Di Mario, M. Valentini, F. Ria, G. Ferraccioli, R. Cimaz y E. Gremese. "FRI0002 Analysis of b cells and t cells subpopulations and collagen specific t cell repertoire in juvenile idiopathic arthritis patients". En Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5415.

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Saito, Takuro, Hiroyoshi Nishikawa, Hisashi Wada, Masaki Mori, Yuichiro Doki y Shimon Sakaguchi. "Abstract B174: FOXP3+CD4+ T-cell subpopulations distinctly control the prognosis of colorectal cancers". En Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b174.

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Dyhre-Petersen, Nanna, Gustav Ørting Jørgensen, Louise Munkholm Andreasson, Trine Hilkjær Petersen, Lisa Pfluger, Alexander Wessely Silberbrandt, Morten Winther Hvidtfeldt, Charlotte Menne Bonefeld, Celeste Porsbjerg y Asger Sverrild. "Effects of blocking TSLP on ILC and T cell subpopulations in patients with asthma". En ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.94.

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Koller, U., I. Pabinger, K. Lechner y W. Knapp. "HEAT INACTIVATED HIGHLY PURIFIED FACTOR VIII CONCENTRATE IN THE TREATMENT OF HEMOPHILIACS". En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644057.

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51 severe hemophiliacs who had previously been treated with not virus-inactivated intermediate purity factor VIII concentrates were divided into two groups according to their immunological status. Group A (n=23) consisted of patients with CD4/CD8 (helper/suppressor) T cell ratio of 1.0, group B (n=28) of . patients with a ratio of 1.0. In patients of group A treatment was switched in May 1983 to highly purified heat inactivated factor VIII concentrate (BEHRINGWERKE GmbH, Marburg) whereas patients of group B continued to receive intermediate purity factor VIII concentrate. In both groups laboratory tests (clinical investigation, routine liver function tests, differential blood count, lymphocyte subpopulations and quantitative immunoglobulin analysis) were performed in May 1983 and repeated 6, 12 and 18 months thereafter. In group A a significant reduction (p 0.005) of CD8 positive cells from 10587/μl (median) to 540/μl (18 months) was observed; no significant changes of CD8 positive cells occurred in group B. CD4/CD8 ratio rose from 0.58 to 0.86 in group A (p = 0.005) and remained unchanged in group B (1.38 versus 1.23). Serum IgG decreased in both groups but was more pronounced in group A. Thus treatment with heat inactivated highly purified factor VIII improved the immunological status of hemophiliacs with an inverse ratio. Retrospective analysis of antibodies to HIV, however, showed that most of the patients of group A were antibody positive (n=21), but the 2 negative patients remained negative. In group B of the 10 HIV negative patients one became positive, all others did not change. Whether this improvement of immunological laboratory findings is of clinical relevance, remains to be established, particularly with respect to the high incidence of antibody positive patients within group A.
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Xu, Qing, BaiHua Cheng y Songlin Xu. "Effects of diode laser ILIB on peripheral blood T lymphocyte subpopulations and NK cells". En 1997 Shanghai International Conference on Laser Medicine and Surgery, editado por Jing Zhu. SPIE, 1998. http://dx.doi.org/10.1117/12.330179.

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Santinon, François, Maxime Batignes, Charlotte Pouchy, Benoit Salomon, Patrice Decker, Marie-Christophe Boissier, Luca Semerano y Natacha Bessis. "03.12 Tnfr2+regulatory t cells subpopulations are highly suppressive and are increased on anti-tnf treatment". En 37th European Workshop for Rheumatology Research 2–4 March 2017 Athens, Greece. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2016-211049.12.

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Zhu, Jing y Fan Ni. "The effects of ILLLI on peripheral blood T lymphocytes subpopulation and NK cells in psoriasis treatment". En 2004 Shanghai international Conference on Laser Medicine and Surgery, editado por Jing Zhu. SPIE, 2005. http://dx.doi.org/10.1117/12.639326.

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Informes sobre el tema "T-cell subpopulations"

1

Splitter, Gary, Zeev Trainin y Yacov Brenner. Lymphocyte Response to Genetically Engineered Bovine Leukemia Virus Proteins in Persistently Lymphocytic Cattle from Israel and the U.S. United States Department of Agriculture, julio de 1995. http://dx.doi.org/10.32747/1995.7570556.bard.

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The goal of this proposal was to identify proteins of BLV recognized by lymphocyte subpopulations and determine the contribution of these proteins to viral pathogenesis. Our hypothesis was that BLV pathogenesis is governed by the T-cell response and that the immune system likely plays an important role in controlling the utcome of infection. Our studies presented in ths final report demonstrate that T cell competency declines with advancing stages of infection. Dramatic differences were observed in lymphocyte proliferation to recombinant proteins encoded by BLV gag (p12, p15, and p24) and env (gp30 and gp15) genes in different disease stages. Because retroviruses are known to mutate frequently, examinatin of infected cattle from both Israel and the United States will likely detect variability in the immune response. This combined research approach provides the first opportunity to selectively address the importance of T-cell proliferation to BLV proteins and cytokines produced during different stages of BLV infection. Lack of this information regarding BLV infection has hindered understanding lympocyte regulation of BLV pathogenesis. We have developed the essential reagents necessary to determine the prominence of different lymphocyte subpopulations and cytokines produced during the different disease stages within the natural host. We found that type 1 cytokines (IL-2 and IFN-g) increased in PBMCs from animals in early disease, and decreasd in PBMCs from animals in late disease stages of BLV infection, while IL-10, increased with disease progression. Recently, a dichotomy between IL-12 and IL-10 has emerged in regards to progression of a variety of diseases. IL-12 activates type 1 cytokine production and has an antagonistic effect on type 2 cytokines. Here, using quantitative competitive PCR, we show that peripheral blood mononuclear cells from bovine leukemia virus infected animals in the alymphocytotic disease stage express increased amount of IL-12 p40 mRNA. In contrast, IL-12 p40 mRNA expression by PL animals was significantly decreased compared to normal and alymphocytotic animals. To examine the functions of these cytokines on BLV expression, BLV tax and pol mRNA expression and p24 protein production were quantified by competitive PCR, and by immunoblotting, respectively. IL-10 inhibited BLV tax and pol mRNA expression by BLV-infected PBMCs. In addition, we determined that macrophages secret soluble factor(s) that activate BLV expression, and that secretion of the soluble factor(s) could be inhibited by IL-10. In contrast, IL-2 increased BLV tax and pol mRNA, and p24 protein production. These findings suggest that macrophages have a key role in regulating BLV expression, and IL-10 produced by BLV-infected animals in late disease stages may serve to control BLV expression, while IL-2 in the early stage of disease may activate BLV expression. PGE2 is an important immune regulator produced only by macrophages, and is known to facilitate HIV replication. We hypothesized that PGE2 may regulate BLV expression. Here, we show that cyclooxygenase-2 (COX-2) mRNA expression was decreased in PBMCs treated with IL-10, while IL-2 enhanced COX-2 mRNA expression. In contrast, addition of PGE2 stimulated BLV tax and pol mRNA expression. In addition, the specific COX-2 inhibitor, NS-398, inhibited BLV expression, while addition of PGE2 increased BLV tax expression regardless of NS-398. These findings suggest that macrophage derived cyclooxygenase -2 products, such as PGE2, may regulate virus expression and disease rogression in BLV infection, and that cytokines (IL-2 and IL-10) may regulate BLV expression through PGE2 production.
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