The Experts below are selected from a list of 72 Experts worldwide ranked by ideXlab platform
O Viale - One of the best experts on this subject based on the ideXlab platform.
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Alloantigen Recognition by two human natural killer cell clones is associated with hla c or a closely linked gene
Proceedings of the National Academy of Sciences of the United States of America, 1992Co-Authors: Marco Colonna, T Spies, Jack L Strominger, Ermanno Ciccone, Alessandro Moretta, Lorenzo Moretta, Daniela Pende, O VialeAbstract:Human natural killer (NK) cells with the CD3- CD16+ phenotype recognize allospecificities on normal T-cell blasts. The NK-defined specificity 1 (NK-1) is recessively inherited and has been mapped to the major histocompatibility complex between the complement gene cluster and HLA-A. A gene for NK-1, however, has not been identified. Here we demonstrate that NK-1 and the recently defined NK specificity 2 (NK-2) are reciprocally associated with homozygosity for a diallelic polymorphism at amino acid positions 77 and 80 in the putative peptide-binding site of HLA-C (P less than 10(-5)). NK-cell Recognition of allogeneic cells may, therefore, be controlled by HLA-C itself or by a closely linked gene(s), which dominantly prevents (resistance alleles) or recessively permits (susceptibility alleles) Recognition of still-unknown target determinants.
Mark D Okusa - One of the best experts on this subject based on the ideXlab platform.
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activation of adenosine 2a receptors attenuates allograft rejection and Alloantigen Recognition
Journal of Immunology, 2007Co-Authors: Charles P Sevigny, Li Li, Alaa S Awad, Liping Huang, Marcia Mcduffie, Joel Linden, Peter I Lobo, Mark D OkusaAbstract:The current studies investigated the in vitro and in vivo effect of adenosine 2A receptor (A2AR) agonists to attenuate allogenic immune activation. We performed MLRs with spleen T lymphocytes and APCs isolated from wild-type and A2AR knockout mice of both C57BL/6 and BALB/c background strains. Two-way MLR-stimulated T cell proliferation was reduced by ATL313, a selective A2AR agonist in a dose-responsive manner (∼70%; 10 nM), an effect reversed by the A2AR antagonist ZM241385 (100 nM). By one-way MLRs, we observed that ATL313’s inhibitory effect was due to effects on both T cells and APCs. ATL313 suppressed the activation markers CD25 and CD40L and the release of inflammatory cytokines IFN-γ, RANTES, IL-12P70, and IL-2. ATL313 also increased negative costimulatory molecules programmed death-1 and CTLA-4 expressed on T cells. In lymphocytes activated with anti-CD3e mAb, ATL313 inhibited the phosphorylation of Zap70, an effect that was reversed by the protein kinase A inhibitor H-89. In skin transplants, allograft survival was enhanced with ATL313, an effect blocked by ZM241385. These results indicate that A2AR agonists attenuate allogenic Recognition by action on both T lymphocytes and APCs in vitro and delayed acute rejection in vivo. We conclude that A2AR agonists may represent a new class of compounds for induction therapy in organ transplantation.
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activation of adenosine 2a receptors attenuates allograft rejection and Alloantigen Recognition
Journal of Immunology, 2007Co-Authors: Charles P Sevigny, Alaa S Awad, Liping Huang, Marcia Mcduffie, Joel Linden, Peter I Lobo, Mark D OkusaAbstract:The current studies investigated the in vitro and in vivo effect of adenosine 2A receptor (A(2A)R) agonists to attenuate allogenic immune activation. We performed MLRs with spleen T lymphocytes and APCs isolated from wild-type and A(2A)R knockout mice of both C57BL/6 and BALB/c background strains. Two-way MLR-stimulated T cell proliferation was reduced by ATL313, a selective A(2A)R agonist in a dose-responsive manner (approximately 70%; 10 nM), an effect reversed by the A(2A)R antagonist ZM241385 (100 nM). By one-way MLRs, we observed that ATL313's inhibitory effect was due to effects on both T cells and APCs. ATL313 suppressed the activation markers CD25 and CD40L and the release of inflammatory cytokines IFN-gamma, RANTES, IL-12P(70), and IL-2. ATL313 also increased negative costimulatory molecules programmed death-1 and CTLA-4 expressed on T cells. In lymphocytes activated with anti-CD3e mAb, ATL313 inhibited the phosphorylation of Zap70, an effect that was reversed by the protein kinase A inhibitor H-89. In skin transplants, allograft survival was enhanced with ATL313, an effect blocked by ZM241385. These results indicate that A(2A)R agonists attenuate allogenic Recognition by action on both T lymphocytes and APCs in vitro and delayed acute rejection in vivo. We conclude that A(2A)R agonists may represent a new class of compounds for induction therapy in organ transplantation.
Marco Colonna - One of the best experts on this subject based on the ideXlab platform.
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Alloantigen Recognition by two human natural killer cell clones is associated with hla c or a closely linked gene
Proceedings of the National Academy of Sciences of the United States of America, 1992Co-Authors: Marco Colonna, T Spies, Jack L Strominger, Ermanno Ciccone, Alessandro Moretta, Lorenzo Moretta, Daniela Pende, O VialeAbstract:Human natural killer (NK) cells with the CD3- CD16+ phenotype recognize allospecificities on normal T-cell blasts. The NK-defined specificity 1 (NK-1) is recessively inherited and has been mapped to the major histocompatibility complex between the complement gene cluster and HLA-A. A gene for NK-1, however, has not been identified. Here we demonstrate that NK-1 and the recently defined NK specificity 2 (NK-2) are reciprocally associated with homozygosity for a diallelic polymorphism at amino acid positions 77 and 80 in the putative peptide-binding site of HLA-C (P less than 10(-5)). NK-cell Recognition of allogeneic cells may, therefore, be controlled by HLA-C itself or by a closely linked gene(s), which dominantly prevents (resistance alleles) or recessively permits (susceptibility alleles) Recognition of still-unknown target determinants.
Lorenzo Moretta - One of the best experts on this subject based on the ideXlab platform.
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Alloantigen Recognition by two human natural killer cell clones is associated with hla c or a closely linked gene
Proceedings of the National Academy of Sciences of the United States of America, 1992Co-Authors: Marco Colonna, T Spies, Jack L Strominger, Ermanno Ciccone, Alessandro Moretta, Lorenzo Moretta, Daniela Pende, O VialeAbstract:Human natural killer (NK) cells with the CD3- CD16+ phenotype recognize allospecificities on normal T-cell blasts. The NK-defined specificity 1 (NK-1) is recessively inherited and has been mapped to the major histocompatibility complex between the complement gene cluster and HLA-A. A gene for NK-1, however, has not been identified. Here we demonstrate that NK-1 and the recently defined NK specificity 2 (NK-2) are reciprocally associated with homozygosity for a diallelic polymorphism at amino acid positions 77 and 80 in the putative peptide-binding site of HLA-C (P less than 10(-5)). NK-cell Recognition of allogeneic cells may, therefore, be controlled by HLA-C itself or by a closely linked gene(s), which dominantly prevents (resistance alleles) or recessively permits (susceptibility alleles) Recognition of still-unknown target determinants.
T Spies - One of the best experts on this subject based on the ideXlab platform.
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Alloantigen Recognition by two human natural killer cell clones is associated with hla c or a closely linked gene
Proceedings of the National Academy of Sciences of the United States of America, 1992Co-Authors: Marco Colonna, T Spies, Jack L Strominger, Ermanno Ciccone, Alessandro Moretta, Lorenzo Moretta, Daniela Pende, O VialeAbstract:Human natural killer (NK) cells with the CD3- CD16+ phenotype recognize allospecificities on normal T-cell blasts. The NK-defined specificity 1 (NK-1) is recessively inherited and has been mapped to the major histocompatibility complex between the complement gene cluster and HLA-A. A gene for NK-1, however, has not been identified. Here we demonstrate that NK-1 and the recently defined NK specificity 2 (NK-2) are reciprocally associated with homozygosity for a diallelic polymorphism at amino acid positions 77 and 80 in the putative peptide-binding site of HLA-C (P less than 10(-5)). NK-cell Recognition of allogeneic cells may, therefore, be controlled by HLA-C itself or by a closely linked gene(s), which dominantly prevents (resistance alleles) or recessively permits (susceptibility alleles) Recognition of still-unknown target determinants.