The proper physiological functioning of most eukaryotic cells requires their assembly into multi-cellular tissues that form organized organ systems. Cells of the immune system develop in bone marrow and lymphoid organs, but as the cells mature they leave these organs and circulate as single cells. Antigen receptors (TCRs) of T cells search for membrane MHC proteins that are bound to peptides derived from infectious pathogens or cellular transformations. The detection of such speci?c peptide–MHC antigens initiates T cell activation, adhesion, and immune-effectors functions. Studies of normal and transformed T cell lines and of T cells from transgenic mice led to comprehensive understanding of the mole- lar basis of antigen-receptor recognition and signaling. In spite of these remarkable genetic and biochemical advances, other key physiological mechanisms that par- cipate in sensing and decoding the immune context to induce the appropriate cellular immune responses remain unresolved. TCRrecognition is tightly regulated to trigger sensitive but balanced T cell responses that result in the effective elimination of the pathogens while minimizing collateral damage to the host. The sensitivity of TCR recognition has to be properly tempered to prevent unintended activation by self-peptide–MHC complexes that cause autoimmune diseases. It is likely that once the TCR is engaged by a peptide– MHC and TCR signaling begins, additional regulatory mechanisms, involving other receptors, would increase the ?delity of the response.
Les informations fournies dans la section « Synopsis » peuvent faire référence à une autre édition de ce titre.
While the importance of the immune synapse as a dynamic cell junction that regulates intercellular communication and viral transmission is universally recognized, many of quantitative and qualitative details remain unsettled. The plasticity of this cell junction has to accommodate many very different binding partners and control the fate of interacting cells. It is likely that developmental changes in the state of the T cells or the APCs can impact the structure of the synapse. It is hoped that uncovering the ordered molecular rearrangement at the membrane will provide the long sought after clues for the remarkable functional sensitivity of T lymphocytes. These dynamic molecular interactions may eventually explain how engagement of the same TCR can generate different outcomes that resolve the immune challenges. The reviews in this issue present a broad slice of the many diverse topics that are currently intensely debated.
Les informations fournies dans la section « A propos du livre » peuvent faire référence à une autre édition de ce titre.
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Taschenbuch. Etat : Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -The proper physiological functioning of most eukaryotic cells requires their assembly into multi-cellular tissues that form organized organ systems. Cells of the immune system develop in bone marrow and lymphoid organs, but as the cells mature they leave these organs and circulate as single cells. Antigen receptors (TCRs) of T cells search for membrane MHC proteins that are bound to peptides derived from infectious pathogens or cellular transformations. The detection of such speci c peptide-MHC antigens initiates T cell activation, adhesion, and immune-effectors functions. Studies of normal and transformed T cell lines and of T cells from transgenic mice led to comprehensive understanding of the mole- lar basis of antigen-receptor recognition and signaling. In spite of these remarkable genetic and biochemical advances, other key physiological mechanisms that par- cipate in sensing and decoding the immune context to induce the appropriate cellular immune responses remain unresolved. TCR recognition is tightly regulated to trigger sensitive but balanced T cell responses that result in the effective elimination of the pathogens while minimizing collateral damage to the host. The sensitivity of TCR recognition has to be properly tempered to prevent unintended activation by self-peptide-MHC complexes that cause autoimmune diseases. It is likely that once the TCR is engaged by a peptide- MHC and TCR signaling begins, additional regulatory mechanisms, involving other receptors, would increase the delity of the response. 272 pp. Englisch. N° de réf. du vendeur 9783642261855
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Taschenbuch. Etat : Neu. Immunological Synapse | Takashi Saito (u. a.) | Taschenbuch | Current Topics in Microbiology and Immunology | xv | Englisch | 2012 | Springer | EAN 9783642261855 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu. N° de réf. du vendeur 106599092
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Taschenbuch. Etat : Neu. Druck auf Anfrage Neuware - Printed after ordering - The proper physiological functioning of most eukaryotic cells requires their assembly into multi-cellular tissues that form organized organ systems. Cells of the immune system develop in bone marrow and lymphoid organs, but as the cells mature they leave these organs and circulate as single cells. Antigen receptors (TCRs) of T cells search for membrane MHC proteins that are bound to peptides derived from infectious pathogens or cellular transformations. The detection of such speci c peptide-MHC antigens initiates T cell activation, adhesion, and immune-effectors functions. Studies of normal and transformed T cell lines and of T cells from transgenic mice led to comprehensive understanding of the mole- lar basis of antigen-receptor recognition and signaling. In spite of these remarkable genetic and biochemical advances, other key physiological mechanisms that par- cipate in sensing and decoding the immune context to induce the appropriate cellular immune responses remain unresolved. TCRrecognition is tightly regulated to trigger sensitive but balanced T cell responses that result in the effective elimination of the pathogens while minimizing collateral damage to the host. The sensitivity of TCR recognition has to be properly tempered to prevent unintended activation by self-peptide-MHC complexes that cause autoimmune diseases. It is likely that once the TCR is engaged by a peptide- MHC and TCR signaling begins, additional regulatory mechanisms, involving other receptors, would increase the delity of the response. N° de réf. du vendeur 9783642261855
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Taschenbuch. Etat : Neu. This item is printed on demand - Print on Demand Titel. Neuware -The proper physiological functioning of most eukaryotic cells requires their assembly into multi-cellular tissues that form organized organ systems. Cells of the immune system develop in bone marrow and lymphoid organs, but as the cells mature they leave these organs and circulate as single cells. Antigen receptors (TCRs) of T cells search for membrane MHC proteins that are bound to peptides derived from infectious pathogens or cellular transformations. The detection of such speci c peptide¿MHC antigens initiates T cell activation, adhesion, and immune-effectors functions. Studies of normal and transformed T cell lines and of T cells from transgenic mice led to comprehensive understanding of the mole- lar basis of antigen-receptor recognition and signaling. In spite of these remarkable genetic and biochemical advances, other key physiological mechanisms that par- cipate in sensing and decoding the immune context to induce the appropriate cellular immune responses remain unresolved. TCRrecognition is tightly regulated to trigger sensitive but balanced T cell responses that result in the effective elimination of the pathogens while minimizing collateral damage to the host. The sensitivity of TCR recognition has to be properly tempered to prevent unintended activation by self-peptide¿MHC complexes that cause autoimmune diseases. It is likely that once the TCR is engaged by a peptide¿ MHC and TCR signaling begins, additional regulatory mechanisms, involving other receptors, would increase the delity of the response.Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg 272 pp. Englisch. N° de réf. du vendeur 9783642261855
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