The Experts below are selected from a list of 12153 Experts worldwide ranked by ideXlab platform
Lewis L Lanier - One of the best experts on this subject based on the ideXlab platform.
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involvement of cd28 in mhc unrestricted cytotoxicity mediated by a human natural killer leukemia cell line
Journal of Immunology, 1992Co-Authors: Miyuki Azuma, Joseph H. Phillips, Mark Cayabyab, D W Buck, Lewis L LanierAbstract:NK cells and certain CTL can recognize and lyse targets without restriction by the MHC. NK cells do not express CD3/TCR complexes and the membrane receptors participating in MHC-unrestricted cytotoxicity are largely unknown. We demonstrate that YT2C2, a human NK leukemia cell line, expresses the CD28 differentiation Ag and can spontaneously lyse both murine and human cell lines expressing B7, a B cell- activation Ag that is a ligand for CD28. The participation of CD28/B7 interactions in MHC-unrestricted cytotoxicity mediated by YT2C2 cells was demonstrated by correlation of target sensitivity with levels of B7 expression, inhibition of cytotoxicity by anti-CD28 or anti-B7 mAb, and by making both murine and human cell lines susceptible to YT2C2-mediated lysis by Genetic Transfection with expression vectors containing B7 cDNA. However, CD28/B7 interactions alone were insufficient to initiate cytotoxicity. mAb inhibition experiments and selection of CD54- (intercellular adhesion molecule-1) deficient B cell targets indicated that CD11a/18 (lymphocyte function-associated Ag-1) also cooperated in CD28/B7-dependent cytotoxicity. The requirement for both CD28/B7 and lymphocyte function-associated Ag-1/intercellular adhesion molecule-1 interactions in YT2C2-mediated MHC-unrestricted cytotoxicity was confirmed by demonstrating that efficient lysis of murine L cells required coTransfection with both B7 and intercellular adhesion molecule-1. These findings support the concept that MHC-unrestricted cytotoxicity may not be due to a unique receptor, but may result from interactions between an appropriate array of "adhesion" molecules with their ligands.
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cd28 interaction with b7 costimulates primary allogeneic proliferative responses and cytotoxicity mediated by small resting t lymphocytes
Journal of Experimental Medicine, 1992Co-Authors: Miyuki Azuma, Joseph H. Phillips, Mark Cayabyab, David Buck, Lewis L LanierAbstract:Engagement of the CD3/T cell antigen receptor complex on small, resting T cells is insufficient to trigger cell-mediated cytotoxicity or to induce a proliferative response. In the present study, we have used Genetic Transfection to demonstrate that interaction of the B7-BB1 B cell activation antigen with the CD28 T cell differentiation antigen costimulates cell-mediated cytotoxicity and proliferation initiated by either anti-CD2 or anti-CD3 monoclonal antibody (mAb). Moreover, a B7-negative Burkitt's lymphoma cell line that fails to stimulate an allogeneic mixed lymphocyte response is rendered a potent stimulator after Transfection with B7. The mixed leukocyte reaction proliferative response against the B7 transfectant is inhibited by either anti-CD28 or B7 mAb. We also demonstrate that freshly isolated small, resting human T cells can mediate anti-CD3 or anti-CD2 mAb-redirected cytotoxicity against a murine Fc receptor-bearing mastocytoma transfected with human B7. These preexisting cytotoxic T lymphocytes in peripheral blood are present in both the CD4 and CD8 subsets, but are preferentially within the CD45RO+ "memory" population. While small, resting T cells apparently require costimulation by CD28/B7 interactions, this requirement is lost after T cell activation. Anti-CD3 initiates a cytotoxic response mediated by in vitro cultured T cell clones in the absence of B7 ligand. The existence of functional cytolytic T cells in the small, resting T cell population may be advantageous in facilitating rapid responses to immune challenge.
Torben Moos - One of the best experts on this subject based on the ideXlab platform.
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nanoparticle derived non viral Genetic Transfection at the blood brain barrier to enable neuronal growth factor delivery by secretion from brain endothelium
Current Medicinal Chemistry, 2011Co-Authors: Louiza Bohn Thomsen, Annette Burkhart Larsen, Jacek Lichota, Torben MoosAbstract:Brain capillary endothelial cells form the blood-brain barrier (BBB) that denotes a major restraint for drug entry to the brain. The identification of many new targets to treat diseases in the brain demands novel thinking in drug design as new therapeutics could often be proteins and molecules of Genetic origins like siRNA, miRNA and cDNA. Such molecules are otherwise prevented from entry into the brain unless encapsulated in drug carriers. The desirable entry of such large, hydrophilic molecules should be made by formulation of particular drug carriers that will enable their transport into the brain endothelium, or even through the endothelium and into the brain. This manuscript reviews the potential of different drug-carriers for therapy to the brain with respect to their targetability, biocompatibility, toxicity and biodegradability.
Anthony S Fargnoli - One of the best experts on this subject based on the ideXlab platform.
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effects of Genetic Transfection on calcium cycling pathways mediated by double stranded adeno associated virus in postinfarction remodeling
The Journal of Thoracic and Cardiovascular Surgery, 2020Co-Authors: Michael G Katz, Sarah M Gubara, Yoav Hadas, Thomas Weber, Arvind Kumar, Efrat Eliyahu, Charles R Bridges, Anthony S FargnoliAbstract:Abstract Objective Restoring calcium sensor protein (S100A1) activity in failing hearts poses a promising therapeutic strategy. We hypothesize that cardiac overexpression of the S100A1 gene mediated by a double-stranded adeno-associated virus (scAAV) results in better functional and molecular improvements compared with the single-stranded virus (ssAAV). Methods Heart failure was induced by coronary artery ligation. Then, intramyocardial injections of saline, AAV9 empty capsid, scAAV9.S100A1, and ssAAV9.S100A1 were performed. Ten weeks postinfarction, all rats received cardiac evaluation; serum and tissue were collected for Genetic analysis, cytokine profiling, and assessments of mitochondrial function and structure. Results Overexpression of AAV9.S100A1 improved systolic and diastolic function. Compared with control, ejection fraction was greater in treated groups (54.8% vs 32.3%, P Conclusions Gene therapy of S100A1 can prevent pathologic postmyocardial infarction remodeling and decrease inflammatory response in ischemic heart failure.
Miyuki Azuma - One of the best experts on this subject based on the ideXlab platform.
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involvement of cd28 in mhc unrestricted cytotoxicity mediated by a human natural killer leukemia cell line
Journal of Immunology, 1992Co-Authors: Miyuki Azuma, Joseph H. Phillips, Mark Cayabyab, D W Buck, Lewis L LanierAbstract:NK cells and certain CTL can recognize and lyse targets without restriction by the MHC. NK cells do not express CD3/TCR complexes and the membrane receptors participating in MHC-unrestricted cytotoxicity are largely unknown. We demonstrate that YT2C2, a human NK leukemia cell line, expresses the CD28 differentiation Ag and can spontaneously lyse both murine and human cell lines expressing B7, a B cell- activation Ag that is a ligand for CD28. The participation of CD28/B7 interactions in MHC-unrestricted cytotoxicity mediated by YT2C2 cells was demonstrated by correlation of target sensitivity with levels of B7 expression, inhibition of cytotoxicity by anti-CD28 or anti-B7 mAb, and by making both murine and human cell lines susceptible to YT2C2-mediated lysis by Genetic Transfection with expression vectors containing B7 cDNA. However, CD28/B7 interactions alone were insufficient to initiate cytotoxicity. mAb inhibition experiments and selection of CD54- (intercellular adhesion molecule-1) deficient B cell targets indicated that CD11a/18 (lymphocyte function-associated Ag-1) also cooperated in CD28/B7-dependent cytotoxicity. The requirement for both CD28/B7 and lymphocyte function-associated Ag-1/intercellular adhesion molecule-1 interactions in YT2C2-mediated MHC-unrestricted cytotoxicity was confirmed by demonstrating that efficient lysis of murine L cells required coTransfection with both B7 and intercellular adhesion molecule-1. These findings support the concept that MHC-unrestricted cytotoxicity may not be due to a unique receptor, but may result from interactions between an appropriate array of "adhesion" molecules with their ligands.
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cd28 interaction with b7 costimulates primary allogeneic proliferative responses and cytotoxicity mediated by small resting t lymphocytes
Journal of Experimental Medicine, 1992Co-Authors: Miyuki Azuma, Joseph H. Phillips, Mark Cayabyab, David Buck, Lewis L LanierAbstract:Engagement of the CD3/T cell antigen receptor complex on small, resting T cells is insufficient to trigger cell-mediated cytotoxicity or to induce a proliferative response. In the present study, we have used Genetic Transfection to demonstrate that interaction of the B7-BB1 B cell activation antigen with the CD28 T cell differentiation antigen costimulates cell-mediated cytotoxicity and proliferation initiated by either anti-CD2 or anti-CD3 monoclonal antibody (mAb). Moreover, a B7-negative Burkitt's lymphoma cell line that fails to stimulate an allogeneic mixed lymphocyte response is rendered a potent stimulator after Transfection with B7. The mixed leukocyte reaction proliferative response against the B7 transfectant is inhibited by either anti-CD28 or B7 mAb. We also demonstrate that freshly isolated small, resting human T cells can mediate anti-CD3 or anti-CD2 mAb-redirected cytotoxicity against a murine Fc receptor-bearing mastocytoma transfected with human B7. These preexisting cytotoxic T lymphocytes in peripheral blood are present in both the CD4 and CD8 subsets, but are preferentially within the CD45RO+ "memory" population. While small, resting T cells apparently require costimulation by CD28/B7 interactions, this requirement is lost after T cell activation. Anti-CD3 initiates a cytotoxic response mediated by in vitro cultured T cell clones in the absence of B7 ligand. The existence of functional cytolytic T cells in the small, resting T cell population may be advantageous in facilitating rapid responses to immune challenge.
Louiza Bohn Thomsen - One of the best experts on this subject based on the ideXlab platform.
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nanoparticle derived non viral Genetic Transfection at the blood brain barrier to enable neuronal growth factor delivery by secretion from brain endothelium
Current Medicinal Chemistry, 2011Co-Authors: Louiza Bohn Thomsen, Annette Burkhart Larsen, Jacek Lichota, Torben MoosAbstract:Brain capillary endothelial cells form the blood-brain barrier (BBB) that denotes a major restraint for drug entry to the brain. The identification of many new targets to treat diseases in the brain demands novel thinking in drug design as new therapeutics could often be proteins and molecules of Genetic origins like siRNA, miRNA and cDNA. Such molecules are otherwise prevented from entry into the brain unless encapsulated in drug carriers. The desirable entry of such large, hydrophilic molecules should be made by formulation of particular drug carriers that will enable their transport into the brain endothelium, or even through the endothelium and into the brain. This manuscript reviews the potential of different drug-carriers for therapy to the brain with respect to their targetability, biocompatibility, toxicity and biodegradability.