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      Viral Interference with Functions of the Cellular Receptor Tyrosine Phosphatase CD45

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          Abstract

          The receptor tyrosine phosphatase CD45 is expressed on the surface of almost all cells of hematopoietic origin. CD45 functions are central to the development of T cells and determine the threshold at which T and B lymphocytes can become activated. Given this pivotal role of CD45 in the immune system, it is probably not surprising that viruses interfere with the activity of CD45 in lymphocytes to dampen the immune response and that they also utilize this molecule to accomplish their replication cycle. Here we report what is known about the interaction of viral proteins with CD45. Moreover, we debate putative interactions of viruses with CD45 in myeloid cells and the resulting consequences—subjects that remain to be investigated. Finally, we summarize the evidence that pathogens were the driving force for the evolution of CD45.

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          Most cited references80

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          An integrated view of protein evolution.

          Why do proteins evolve at different rates? Advances in systems biology and genomics have facilitated a move from studying individual proteins to characterizing global cellular factors. Systematic surveys indicate that protein evolution is not determined exclusively by selection on protein structure and function, but is also affected by the genomic position of the encoding genes, their expression patterns, their position in biological networks and possibly their robustness to mistranslation. Recent work has allowed insights into the relative importance of these factors. We discuss the status of a much-needed coherent view that integrates studies on protein evolution with biochemistry and functional and structural genomics.
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            T cell receptor signalling networks: branched, diversified and bounded.

            Engagement of antigen-specific T cell receptors (TCRs) is a prerequisite for T cell activation. Acquisition of appropriate effector T cell function requires the participation of multiple signals from the T cell microenvironment. Trying to understand how these signals integrate to achieve specific functional outcomes while maintaining tolerance to self is a major challenge in lymphocyte biology. Several recent publications have provided important insights into how dysregulation of T cell signalling and the development of autoreactivity can result if the branching and integration of signalling pathways are perturbed. We discuss how these findings highlight the importance of spatial segregation of individual signalling components as a way of regulating T cell responsiveness and immune tolerance.
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              Function of the Src-family kinases, Lck and Fyn, in T-cell development and activation.

              The function of the Src-family kinases (SFKs) Lck and Fyn in T cells has been intensively studied over the past 15 years. Animal models and cell line studies both indicate a critical role for Lck and Fyn in proximal T-cell antigen receptor (TCR) signal transduction. Recruited SFKs phosphorylate TCR ITAMs (immunoreceptor tyrosine-based activation motifs) in the CD3 and zeta chains, which then serve as docking sites for Syk-family kinases. SFKs then phosphorylate and activate the recruited Syk-family kinase. Lck and Fyn are spatially segregated in cell membranes due to differential lipid raft localization, and may undergo sequential activation. In addition to the CD4 and CD8 coreceptors, a recently described adaptor, Unc119, may link SFKs to the TCR. CD45 and Csk provide positive and negative regulatory control of SFK functions, respectively, and Csk is constitutively bound to the transmembrane adapter protein, PAG/Cbp. TCR-based signaling is required at several stages of T-cell development, including at least pre-TCR signaling, positive selection, peripheral maintenance of naive T cells, and lymphopenia-induced proliferation. SFKs are required for each of these TCR-based signals, and Lck seems to be the major contributor.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Viruses
                Viruses
                viruses
                Viruses
                MDPI
                1999-4915
                23 March 2015
                March 2015
                : 7
                : 3
                : 1540-1557
                Affiliations
                Department of Virology, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany; E-Mails: thiel.nadine@ 123456mh-hannover.de (N.T.); zischke.jasmin@ 123456mh-hannover.de (J.Z.); elbasani.endrit@ 123456mh-hannover.de (E.E.); kay-jackson.penelope@ 123456mh-hannover.de (P.K-F.)
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: messerle.martin@ 123456mh-hannover.de ; Tel.: +49-511-532-4320; Fax: +49-511-532-8736.
                Article
                viruses-07-01540
                10.3390/v7031540
                4379584
                25807057
                6f5fefad-d09e-45c6-adff-ef6c6b74fbc4
                © 2015 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 20 January 2015
                : 19 March 2015
                Categories
                Review

                Microbiology & Virology
                cd45,viral immune modulation,evolution,positive selection
                Microbiology & Virology
                cd45, viral immune modulation, evolution, positive selection

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