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10.1128/JVI.01559-10 http://scihub22266oqcxt.onion/10.1128/JVI.01559-10 C3004299!3004299 !20943986     free     free     free Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 215.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 249.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 249.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 249.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\20943986 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Virol 2010 ; 84 (24 ): 12564-75 Nephropedia Template TP {{tp|p=20943986 |t=2010. Suppression of innate immune pathology by regulatory T cells during Influenza A virus infection of immunodeficient mice |pdf=|usr=}}{{20943986 }} gab.com Text Suppression of innate immune pathology by regulatory T cells during Influenza A virus infection of immunodeficient mice JO: J Virol http://www.kidney.de/pget.php?&tw=1&pmid=20943986 #FOAvip The viral infection of higher vertebrates elicits potent innate and adaptive host immunity. However, an excessive or inappropriate immune response also may lead to host pathology that often is more severe than the direct effects of viral replication. Therefore, several mechanisms exist that regulate the magnitude and class of the immune response. Here, we have examined the potential involvement of regulatory T (Treg) cells in limiting pathology induced by influenza A virus (IAV) infection. Using lymphocyte-deficient mice as hosts, we showed that Treg cell reconstitution resulted in a significant delay in weight loss and prolonged survival following infection. The adoptively transferred Treg cells did not affect the high rate of IAV replication in the lungs of lymphocyte-deficient hosts, and therefore their disease-ameliorating effect was mediated through the suppression of innate immune pathology. Mechanistically, Treg cells reduced the accumulation and altered the distribution of monocytes/macrophages in the lungs of IAV-infected hosts. This reduction in lung monocytosis was associated with a specific delay in monocyte chemotactic protein-2 (MCP-2) induction in the infected lungs. Nevertheless, Treg cells failed to prevent the eventual development of severe disease in lymphocyte-deficient hosts, which likely was caused by the ongoing IAV replication. Indeed, using T-cell-deficient mice, which mounted a T-cell-independent B cell response to IAV, we further showed that the combination of virus-neutralizing antibodies and transferred Treg cells led to the complete prevention of clinical disease following IAV infection. Taken together, these results suggested that innate immune pathology and virus-induced pathology are the two main contributors to pathogenesis during IAV infection. Twit Text FOAVip Suppression of innate immune pathology by regulatory T cells during Influenza A virus infection of immunodeficient mice ????J Virol http://www.kidney.de/pget.php?&tw=1&pmid=20943986 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20943986 #FOAvip English Wikipedia <ref>{{Cite pmid|20943986 }}</ref> Suppression of innate immune pathology by regulatory T cells during Influenza A virus infection of immunodeficient mice #MMPMID20943986 Antunes I ; Kassiotis G J Virol 2010[Dec]; 84 (24 ): 12564-75 PMID20943986 show ga The viral infection of higher vertebrates elicits potent innate and adaptive host immunity. However, an excessive or inappropriate immune response also may lead to host pathology that often is more severe than the direct effects of viral replication. Therefore, several mechanisms exist that regulate the magnitude and class of the immune response. Here, we have examined the potential involvement of regulatory T (Treg) cells in limiting pathology induced by influenza A virus (IAV) infection. Using lymphocyte-deficient mice as hosts, we showed that Treg cell reconstitution resulted in a significant delay in weight loss and prolonged survival following infection. The adoptively transferred Treg cells did not affect the high rate of IAV replication in the lungs of lymphocyte-deficient hosts, and therefore their disease-ameliorating effect was mediated through the suppression of innate immune pathology. Mechanistically, Treg cells reduced the accumulation and altered the distribution of monocytes/macrophages in the lungs of IAV-infected hosts. This reduction in lung monocytosis was associated with a specific delay in monocyte chemotactic protein-2 (MCP-2) induction in the infected lungs. Nevertheless, Treg cells failed to prevent the eventual development of severe disease in lymphocyte-deficient hosts, which likely was caused by the ongoing IAV replication. Indeed, using T-cell-deficient mice, which mounted a T-cell-independent B cell response to IAV, we further showed that the combination of virus-neutralizing antibodies and transferred Treg cells led to the complete prevention of clinical disease following IAV infection. Taken together, these results suggested that innate immune pathology and virus-induced pathology are the two main contributors to pathogenesis during IAV infection. |*Immunity, Innate [MESH] |Animals [MESH] |Antibodies, Neutralizing/pharmacology [MESH] |B-Lymphocytes/immunology/virology [MESH] |Biomarkers, Tumor/genetics/metabolism [MESH] |Blotting, Western [MESH] |Chemokine CCL8/metabolism [MESH] |Chemokines/blood [MESH] |Cytokines/blood [MESH] |Gene Expression Profiling [MESH] |Homeodomain Proteins/physiology [MESH] |Humans [MESH] |Immunoenzyme Techniques [MESH] |Influenza A virus/*immunology [MESH] |Lung Diseases/immunology/*prevention & control/virology [MESH] |Lymphocyte Depletion [MESH] |Macrophages/immunology/virology [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Mice, Nude [MESH] |Monocytes/immunology/virology [MESH] |Oligonucleotide Array Sequence Analysis [MESH] |Orthomyxoviridae Infections/*immunology/pathology/virology [MESH] |RNA, Messenger/genetics [MESH] |Reverse Transcriptase Polymerase Chain Reaction [MESH] |T-Lymphocytes, Regulatory/*immunology/virology [MESH] |T-Lymphocytes/immunology/virology [MESH]Suppression of innate immune pathology by regulatory T cells during In(epmc).pdf DeepDyve Pubget Overpricing