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tcr-t-cell-receptor

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Flow cytometry for CD4<sup>+</sup> (<em>left</em>) and CD8<sup>+</sup>...
Published: 18 October 2013
FIG. 3. Flow cytometry for CD4+ (left) and CD8+ T cells (right). A: Cell counts. B: CD3 occupancy/cell. C: CD3/TCR (T-cell receptor) modulation on cells. D: Percentage of cells positive for Foxp3 marker. Symbols indicate means, and bars indicate standard errors. A and C: Number of patients is above (placebo) or below (teplizumab). B and D: Number of patients is above (teplizumab) or below (placebo). FIG. 3. Flow cytometry for CD4+ (left) and CD8+ T cells (right). A: Cell counts. B: CD3 occupancy/cell. C: CD3/TCR (T-cell receptor) modulation on cells. D: Percentage of cells positive for Foxp3 marker. Symbols indicate means, and bars indicate standard errors. A and C: Number of patients is above (placebo) or below (teplizumab). B and D: Number of patients is above (teplizumab) or below (placebo). More
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The model illustrating the metabolic function of B7-1/B7-2 in obesity. The ...
Published: 13 March 2014
Figure 1 The model illustrating the metabolic function of B7-1/B7-2 in obesity. The interactions mediated by the B7-1/B7-2 ligands and the CD28/CTLA-4 receptors are required for the homeostasis and function of Treg cells. Loss of B7-1/B7-2 in mice leads to a systemic reduction of Treg cells, incre... More
Images
Opportunities for individualized therapeutic decision-making using T1D immu...
Published: 16 March 2021
Figure 4 Opportunities for individualized therapeutic decision-making using T1D immune profiles. Targeted therapeutics for particular T or B lymphocytes, specific cytokines, or other selected immune pathways provide alternatives for disease intervention, tailored to individualized patients. Such p... More
Images
Proposed effects of EXOs released by islet MSCs. Although there is the poss...
Published: 13 February 2014
Figure 1 Proposed effects of EXOs released by islet MSCs. Although there is the possibility that EXOs directly stimulate T and B cells, it is likely that EXOs affect DCs that, in turn, initiate anti-β-cell–specific T-cell response. EXOs may lead to the maturation of inflammatory DCs or “feed” DCs ... More
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GAD-reactive <span class="search-highlight">cells</span> stimulated on immunization of young NOD mice with incomp...
Published: 21 May 2011
FIG. 1. GAD-reactive cells stimulated on immunization of young NOD mice with incomplete Freund’s adjuvant and GAD peptide 524-543 produce IL-13. This may have many effects on a variety of tissues that include possible stimulation of a putative regulatory population of cells that expresses IL-13Rα1... More
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Interactions and functions of B <span class="search-highlight">cells</span> that may influence autoimmune diabete...
Published: 15 May 2014
Figure 1 Interactions and functions of B cells that may influence autoimmune diabetes. 1. B cells bind antigen specifically via cell surface immunoglobulin—the specificity of the immunoglobulin directs processing of the protein ( 15 ). 2. The B-cell specificity increases the ability of B cells to present protein antigen to CD4 T cells ( 16 ). 3. B cells enhance antigen presentation to CD8 T cells ( 17 ). 4. B cells may enhance antigen presentation by dendritic cells ( 18 ). 5. B cells differentiate to plasma cells, which produce autoantibodies. MHC, major histocompatibility complex; TCR, T-cell receptor. Figure 1. Interactions and functions of B cells that may influence autoimmune diabetes. 1. B cells bind antigen specifically via cell surface immunoglobulin—the specificity of the immunoglobulin directs processing of the protein (15). 2. The B-cell specificity increases the ability of B cells to present protein antigen to CD4 T cells (16). 3. B cells enhance antigen presentation to CD8 T cells (17). 4. B cells may enhance antigen presentation by dendritic cells (18). 5. B cells differentiate to plasma cells, which produce autoantibodies. MHC, major histocompatibility complex; TCR, T-cell receptor. More
Images
Processing of the PPI signal peptide. Model of PPI signal peptide processin...
Published: 17 January 2018
Figure 6 Processing of the PPI signal peptide. Model of PPI signal peptide processing in which N-terminal peptides may be released by SPP into the cytoplasm, where they depend on TAP transport into the ER and ERAP1 trimming before loading into nascent HLA (illustrated by the example of PPI3–11 loading into HLA-A2402). By contrast, ER luminal peptides are released directly into the ER lumen and do not require TAP transport but equally require trimming by ERAP1 for optimal presentation (illustrated by the example of PPI15–24 loading into HLA-A0201). TCR, T-cell receptor. Figure 6. Processing of the PPI signal peptide. Model of PPI signal peptide processing in which N-terminal peptides may be released by SPP into the cytoplasm, where they depend on TAP transport into the ER and ERAP1 trimming before loading into nascent HLA (illustrated by the example of PPI3–11 loading into HLA-A2402). By contrast, ER luminal peptides are released directly into the ER lumen and do not require TAP transport but equally require trimming by ERAP1 for optimal presentation (illustrated by the example of PPI15–24 loading into HLA-A0201). TCR, T-cell receptor. More
Images
Islets treated with AAGP have decreased oxidative stress. <em>A</em>...
Published: 18 November 2015
Figure 2 Islets treated with AAGP have decreased oxidative stress. A: Human islets in culture had an increased concentration of ROS when treated with Tac. However, supplementation with AAGP significantly decreased this effect (P < 0.05). Oxidative stress was measured by fold increase in extracellular ROS analyzed with the Acridan Lumigen PS-3 assay (n = 5). AAGP effect is not the result of direct drug inhibition with Tac. BD: Allogeneic MLR was used to evaluate direct drug inhibition. Results show a significant decrease of T-cell proliferation in the presence of Tac, AAGP, and the combination of both, hence no direct inhibition of Tac by AAGP. Data are mean ± SEM (n = 6). *P < 0.05, ***P < 0.001, ****P < 0.0001. TCR, T-cell receptor. Figure 2. Islets treated with AAGP have decreased oxidative stress. A: Human islets in culture had an increased concentration of ROS when treated with Tac. However, supplementation with AAGP significantly decreased this effect (P < 0.05). Oxidative stress was measured by fold increase in extracellular ROS analyzed with the Acridan Lumigen PS-3 assay (n = 5). AAGP effect is not the result of direct drug inhibition with Tac. B–D: Allogeneic MLR was used to evaluate direct drug inhibition. Results show a significant decrease of T-cell proliferation in the presence of Tac, AAGP, and the combination of both, hence no direct inhibition of Tac by AAGP. Data are mean ± SEM (n = 6). *P < 0.05, ***P < 0.001, ****P < 0.0001. TCR, T-cell receptor. More
Images
Proposed schematic model of the combined release of autoantigens and proinf...
Published: 21 November 2016
Figure 7 Proposed schematic model of the combined release of autoantigens and proinflammatory ER proteins in β-cell exosomes under cytokine-induced ER stress conditions. ER stress can be induced in pancreatic β-cells by Th1 cytokines and other inflammatory factors, leading to the upregulation of E... More
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Overview of the islet immune platform and its communication with the lympho...
Published: 15 July 2019
Figure 1 Overview of the islet immune platform and its communication with the lymphoid tissues. The pancreatic β-cells contain two sets of vesicles that provide antigenic materials. The regular insulin DCG mainly contains abundant insulin molecules that are secreted to regulate glucose metabolism.... More
Images
Hypothetical mechanisms causing autoimmune pancreatitis. Although the patho...
Published: 01 March 2009
FIG. 1. Hypothetical mechanisms causing autoimmune pancreatitis. Although the pathogenesis of AIP and fulminant type 1 diabetes remains to be elucidated, AIP, similar to other autoimmune diseases, is associated with polymorphisms within the HLA complex. In the Japanese population, the highest risk for autoimmune pancreatitis is conferred by the HLA DRB1*0405-DQB1*0401 haplotype (ref. 11 ). Each allele is simply given a number that represents a unique amino acid sequence, and each sequence binds only certain peptides, which could be amylase α-2A peptides. Antigen-presenting cells (APC) present these peptides to lymphocytes and provide signals that stimulate the proliferation and differentiation of lymphocytes, generally T-lymphocytes. Interestingly, regulatory T-cell–deficient NOD CD28KO mice develop spontaneous AIP, which in this model is not a consequence of preexisting β-cell autoimmunity (ref. 13 ). This mechanism could also play a role in the pathogenesis of AIP in humans. The histologic pattern of AIP in humans includes a periductal collar of lymphoplasmacytic inflammation (arrows, hematoxylin and eosin image reprinted with permission from Finkelbert et al. [ref. 16 ]). MHC, major histocompatibility complex; TCR, T-cell receptor. (Please see http://dx.doi.org/10.2337/db08-1655 for a high-quality digital representation of this figure.) FIG. 1. Hypothetical mechanisms causing autoimmune pancreatitis. Although the pathogenesis of AIP and fulminant type 1 diabetes remains to be elucidated, AIP, similar to other autoimmune diseases, is associated with polymorphisms within the HLA complex. In the Japanese population, the highest risk for autoimmune pancreatitis is conferred by the HLA DRB1*0405-DQB1*0401 haplotype (ref. 11). Each allele is simply given a number that represents a unique amino acid sequence, and each sequence binds only certain peptides, which could be amylase α-2A peptides. Antigen-presenting cells (APC) present these peptides to lymphocytes and provide signals that stimulate the proliferation and differentiation of lymphocytes, generally T-lymphocytes. Interestingly, regulatory T-cell–deficient NOD CD28KO mice develop spontaneous AIP, which in this model is not a consequence of preexisting β-cell autoimmunity (ref. 13). This mechanism could also play a role in the pathogenesis of AIP in humans. The histologic pattern of AIP in humans includes a periductal collar of lymphoplasmacytic inflammation (arrows, hematoxylin and eosin image reprinted with permission from Finkelbert et al. [ref. 16]). MHC, major histocompatibility complex; TCR, T-cell receptor. (Please see http://dx.doi.org/10.2337/db08-1655 for a high-quality digital representation of this figure.) More
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<em>A</em>: Constructs used to generate transgenic mice. The cDNAs ...
Published: 01 July 2005
FIG. 1. A: Constructs used to generate transgenic mice. The cDNAs (below) were cloned separately into the EcoRI site of the vector (top). Arrowheads indicate primer binding sites. Gray shading indicates open reading frames, and black shading indicates the location of epitope tags. Elements are drawn to scale except the H-2Kb promoter. TCR, T-cell receptor. B: Detection of transgene mRNA by RT-PCR of islet total RNA. Primer sets are indicated at the top; the presence of individual transgenes is indicated below (+). Arrows indicate products of the expected size. Each set of reactions is separated by a 100-bp molecular weight ladder. C: Detection of cell surface expression of extracellular (EC) SOD-GPI by flow cytometric analysis. IFN-γ–treated wild-type and extracellular SOD-GPI transgenic splenocytes stained using an antibody to the FLAG epitope tag are indicated by the thin and thick lines, respectively. D: Total SOD and Gpx activity in islet and splenocyte lysates. □, wild type; , extracellular SOD-GPI; ▪, Cu/Zn SOD; , triple-transgenic line C; gray bars, Gpx-1. FIG. 1. A: Constructs used to generate transgenic mice. The cDNAs (below) were cloned separately into the EcoRI site of the vector (top). Arrowheads indicate primer binding sites. Gray shading indicates open reading frames, and black shading indicates the location of epitope tags. Elements are drawn to scale except the H-2Kb promoter. TCR, T-cell receptor. B: Detection of transgene mRNA by RT-PCR of islet total RNA. Primer sets are indicated at the top; the presence of individual transgenes is indicated below (+). Arrows indicate products of the expected size. Each set of reactions is separated by a 100-bp molecular weight ladder. C: Detection of cell surface expression of extracellular (EC) SOD-GPI by flow cytometric analysis. IFN-γ–treated wild-type and extracellular SOD-GPI transgenic splenocytes stained using an antibody to the FLAG epitope tag are indicated by the thin and thick lines, respectively. D: Total SOD and Gpx activity in islet and splenocyte lysates. □, wild type; , extracellular SOD-GPI; ▪, Cu/Zn SOD; , triple-transgenic line C; gray bars, Gpx-1. More
Images
<em>A</em>: Constructs used to generate transgenic mice. The cDNAs ...
Published: 01 July 2005
FIG. 1. A: Constructs used to generate transgenic mice. The cDNAs (below) were cloned separately into the EcoRI site of the vector (top). Arrowheads indicate primer binding sites. Gray shading indicates open reading frames, and black shading indicates the location of epitope tags. Elements are drawn to scale except the H-2Kb promoter. TCR, T-cell receptor. B: Detection of transgene mRNA by RT-PCR of islet total RNA. Primer sets are indicated at the top; the presence of individual transgenes is indicated below (+). Arrows indicate products of the expected size. Each set of reactions is separated by a 100-bp molecular weight ladder. C: Detection of cell surface expression of extracellular (EC) SOD-GPI by flow cytometric analysis. IFN-γ–treated wild-type and extracellular SOD-GPI transgenic splenocytes stained using an antibody to the FLAG epitope tag are indicated by the thin and thick lines, respectively. D: Total SOD and Gpx activity in islet and splenocyte lysates. □, wild type; , extracellular SOD-GPI; ▪, Cu/Zn SOD; , triple-transgenic line C; gray bars, Gpx-1. FIG. 1. A: Constructs used to generate transgenic mice. The cDNAs (below) were cloned separately into the EcoRI site of the vector (top). Arrowheads indicate primer binding sites. Gray shading indicates open reading frames, and black shading indicates the location of epitope tags. Elements are drawn to scale except the H-2Kb promoter. TCR, T-cell receptor. B: Detection of transgene mRNA by RT-PCR of islet total RNA. Primer sets are indicated at the top; the presence of individual transgenes is indicated below (+). Arrows indicate products of the expected size. Each set of reactions is separated by a 100-bp molecular weight ladder. C: Detection of cell surface expression of extracellular (EC) SOD-GPI by flow cytometric analysis. IFN-γ–treated wild-type and extracellular SOD-GPI transgenic splenocytes stained using an antibody to the FLAG epitope tag are indicated by the thin and thick lines, respectively. D: Total SOD and Gpx activity in islet and splenocyte lysates. □, wild type; , extracellular SOD-GPI; ▪, Cu/Zn SOD; , triple-transgenic line C; gray bars, Gpx-1. More
Images
<em>A</em>: Constructs used to generate transgenic mice. The cDNAs ...
Published: 01 July 2005
FIG. 1. A: Constructs used to generate transgenic mice. The cDNAs (below) were cloned separately into the EcoRI site of the vector (top). Arrowheads indicate primer binding sites. Gray shading indicates open reading frames, and black shading indicates the location of epitope tags. Elements are drawn to scale except the H-2Kb promoter. TCR, T-cell receptor. B: Detection of transgene mRNA by RT-PCR of islet total RNA. Primer sets are indicated at the top; the presence of individual transgenes is indicated below (+). Arrows indicate products of the expected size. Each set of reactions is separated by a 100-bp molecular weight ladder. C: Detection of cell surface expression of extracellular (EC) SOD-GPI by flow cytometric analysis. IFN-γ–treated wild-type and extracellular SOD-GPI transgenic splenocytes stained using an antibody to the FLAG epitope tag are indicated by the thin and thick lines, respectively. D: Total SOD and Gpx activity in islet and splenocyte lysates. □, wild type; , extracellular SOD-GPI; ▪, Cu/Zn SOD; , triple-transgenic line C; gray bars, Gpx-1. FIG. 1. A: Constructs used to generate transgenic mice. The cDNAs (below) were cloned separately into the EcoRI site of the vector (top). Arrowheads indicate primer binding sites. Gray shading indicates open reading frames, and black shading indicates the location of epitope tags. Elements are drawn to scale except the H-2Kb promoter. TCR, T-cell receptor. B: Detection of transgene mRNA by RT-PCR of islet total RNA. Primer sets are indicated at the top; the presence of individual transgenes is indicated below (+). Arrows indicate products of the expected size. Each set of reactions is separated by a 100-bp molecular weight ladder. C: Detection of cell surface expression of extracellular (EC) SOD-GPI by flow cytometric analysis. IFN-γ–treated wild-type and extracellular SOD-GPI transgenic splenocytes stained using an antibody to the FLAG epitope tag are indicated by the thin and thick lines, respectively. D: Total SOD and Gpx activity in islet and splenocyte lysates. □, wild type; , extracellular SOD-GPI; ▪, Cu/Zn SOD; , triple-transgenic line C; gray bars, Gpx-1. More
Journal Articles
Journal: Diabetes
Diabetes 2006;55(7):1978–1984
Published: 01 July 2006
... play in the pathogenesis of type 1 diabetes. Both pathogenic and protective T-cell clones recognizing the B:9-23 peptide have been produced. This report describes the successful creation of BDC12-4.1 T-cell receptor (TCR) transgenic mice with spontaneous insulitis in F1 mice (FVB × NOD) and spontaneous...
Meeting Abstracts
Journal: Diabetes
Diabetes 1999;48(1):34–42
Published: 01 January 1999
... understood. We recently established 8.3-T-cell receptor (TCR)-beta transgenic NOD mice that show a selective acceleration of the recruitment of CD8+ T-cells into the islets of prediabetic animals, resulting in rapid beta-cell destruction and early onset of diabetes. This study was initiated to determine...
Journal Articles
Journal: Diabetes
Diabetes 1995;44(3):354–359
Published: 01 March 1995
... by preparing Southern blots of T-cell receptor (TCR) β-chain genes amplified by polymerase chain reaction (PCR) from islets from C57BL/KsJ mice given multiple doses of STZ. The relative abundance of TCR gene products in islets was compared with spleen cells stimulated with anti-CD3 monoclonal antibody (mAb...
Journal Articles
Journal: Diabetes
Diabetes 1994;43(11):1318–1325
Published: 01 November 1994
... antibodies revealed HLA-DQw1-restricted recognition of BMA. An analysis of the T-cell receptor (TCR) repertoire of the T-cell line after 8 and 40 days of culture showed a prominent usage of the Val and Vα12 gene families. Although sequencing of the TCR Vα and Vβ chains of the three clones demonstrated...
Journal Articles
Journal: Diabetes
Diabetes 2008;57(5):1321–1330
Published: 01 May 2008
..., the ability to study these processes using unmanipulated T-cell populations that have a broad range of insulitic and diabetogenic potential has been greatly limited. T-cell receptor (TCR) transgenic (Tg) mice are powerful tools for the analysis of autoimmune diseases such as type 1 diabetes. However, only...
Includes: Supplementary data
Journal Articles
Journal: Diabetes
Diabetes 2001;50(9):1992–2000
Published: 01 September 2001
... induced by transgenic expression of an H2-Db class I−restricted T-cell receptor (TCR) specific for a pathologically irrelevant lymphocytic choriomeningitis virus (LCMV) peptide. TCR allelic exclusion greatly reduced the pool of T-cells from which diabetogenic effectors could be derived...