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Synapse immunological

In the specialized environment of secondary lymphoid tissues such as lymph nodes or spleen, dendritic cells provide the requirements for naive T-lymphocytes to become activated and to proliferate. The professional antigen-presenting cells present peptides in MHC II, express costimulatory molecules, and release cytokines into the immunological synapse, which is formed by the antigen-presenting cell and the naive T-lymphocyte. Thus, cells of innate immunity initiate and facilitate the activation of naive lymphocytes, and it is easily conceivable that their cytokines and adhesion molecules will instruct the naive T-lymphocyte during activation and differentiation to T-effector cells. [Pg.614]

Mossman, K. and Groves, J. (2007) Micropatterned supported membranes as tools for quantitative studies of ihe immunological synapse. Chem. Soc. Rev., 36. 46-54. [Pg.236]

Garcia E, Pion M, Pelchen-Matthews A, et al. HIV-1 trafficking to the dendritic cell-T-cell infectious synapse uses a pathway of tetraspanin sorting to the immunological synapse. Traffic 2005 6(6) 488-501. [Pg.284]

Geyeregger, R. et al., Polyunsaturated fatty acids interfere with formation of the immunological synapse, J Leukoc Biol, 77, 680, 2005. [Pg.202]

Beissert S, Gueler F, Loser K, Gunzer M Naive B cells generate regulatory T cells in the presence of a mature immunologic synapse. Blood 2007 110 1519-1529. [Pg.39]

Fig. 11.1. Principle of an immunological synapse. Possibilities for communication between B and T cells during an immune response. Antigenic peptides are presented by the MHC complex class II at the surface of the B cell. The antigens are recognized and bound by T cell receptors of the T cell. The T cell receptor is activated and sets a signal chain in motion that leads to activation of the expression of cytokines, such as IL-2. The cytokine is secreted, and binds and activates a cytokine receptor on the B cell. TNFa is shown as another example of a ligand-receptor system. TNFa communicates, as a membrane-bound ligand, with a corresponding receptor on the surface of the B cell. The interactions shown take place in a narrow spatial region between B and T cells, which is why this system is referred to as an immunological synapse. TNF tumor necrosis factor MHC major histocompatibility complex IL-2 interleukin 2. Fig. 11.1. Principle of an immunological synapse. Possibilities for communication between B and T cells during an immune response. Antigenic peptides are presented by the MHC complex class II at the surface of the B cell. The antigens are recognized and bound by T cell receptors of the T cell. The T cell receptor is activated and sets a signal chain in motion that leads to activation of the expression of cytokines, such as IL-2. The cytokine is secreted, and binds and activates a cytokine receptor on the B cell. TNFa is shown as another example of a ligand-receptor system. TNFa communicates, as a membrane-bound ligand, with a corresponding receptor on the surface of the B cell. The interactions shown take place in a narrow spatial region between B and T cells, which is why this system is referred to as an immunological synapse. TNF tumor necrosis factor MHC major histocompatibility complex IL-2 interleukin 2.
The generation of peripheral Treg cells may result in the establishment of homeostasis after its disruption. Examples include infection, autoimmune diseases, certain forms of cancers and immunodeficiency syndrome. The mechanisms by which peripheral Treg cells induce self-tolerance and homeostasis may involve cytokines or cell-cell interaction. The cytokines IL-10 and TGF-(3 and molecules such as CTLA-4 are involved in the effector mechanisms of Treg cells. The indirect effects of Treg cells may be mediated via APCs or NK cells. More specifically, the assembly of immunological synapse between APCs and effector cells is modulated by Treg cells, which may be mediated via direct or indirect mechanisms. [Pg.209]

Hiltbold, E.M., Poloso, N.J. and Roche, PA. (2003) MHC class Il-peptide complexes and APC lipid rafts accumulate at the immunological synapse. J. Immunol. 170, 1329-1338. [Pg.126]

Mossman KD, Campi G, Groves JT, Dustin ML. Altered TCR signaling from geometrically repatterned immunological synapses. Science 2005 310 1191-1193. [Pg.982]

Bolte S, Cordelieres FP. A guided tour into subcellular colocahzation analysis in light microscopy. J. Microscopy 2006 224231-224232. Dustin ML. T-cell activation through immunological synapses and kinapses. Immunol. Rev. 2008 221 77-89. [Pg.982]

Schmid DA, Depta JP, LuthI M, PIchler WJ Transfection of drug-specific T-cell receptors Into hybridoma cells tools to monitor drug Interaction with T-cell receptors and evaluate cross-reactivity to related compounds. Mol Pharmacol 2006 70 356-65. Dustin ML, Cooper JA The Immunological synapse and the actin cytoskeleton molecular hardware forT cell signaling. Nat Immunol 2000 1 23-9. [Pg.147]

Grakoui A, Bromley SK, Sumen C, Davis MM, Shaw AS, Allen PM, Dustin ML The immunological synapse a molecular machine controlling T cell activation. Science 1999 285 221-227. [Pg.178]

Darlington P, Baroja M, Chau T, Siu E, Ling V, Carreno B, Madrenas J Surface cytotoxic T lymphocyte-associated antigen 4 partitions within lipid rafts and relocates to the immunological synapse under conditions of inhibition ofT cell activation. J Exp Med 2002 195 1-12. [Pg.178]


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See also in sourсe #XX -- [ Pg.359 ]

See also in sourсe #XX -- [ Pg.1835 ]




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