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10.1128/JVI.75.21.10460-10466.2001 http://scihub22266oqcxt.onion/10.1128/JVI.75.21.10460-10466.2001 C114620!114620!11581414     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Virol 2001 ; 75 (21): 10460-6 Nephropedia Template TP {{tp|p=11581414|t=2001. CD8+ T Lymphocytes Mediate Borna Disease Virus-Induced Immunopathology Independently of Perforin |pdf=|usr=}}{{11581414}} gab.com Text CD8+ T Lymphocytes Mediate Borna Disease Virus-Induced Immunopathology Independently of Perforin JO: J Virol http://www.kidney.de/pget.php?&tw=1&pmid=11581414 #FOAvip Perforin-mediated lysis of target cells is the major antiviral effector mechanism of CD8+ T lymphocytes. We have analyzed the role of perforin in a mouse model for CD8+ T-cell-mediated central nervous system (CNS) immunopathology induced by Borna disease virus. When a defective perforin gene was introduced into the genetic background of the Borna disease-susceptible mouse strain MRL, the resulting perforin-deficient mice developed strong neurological disease in response to infection indistinguishable from that of their perforin-expressing littermates. The onset of disease was slightly delayed. Brains of diseased perforin-deficient mice showed similar amounts and a similar distribution of CD8+ T cells as wild-type animals. Perforin deficiency had no impact on the kinetics of viral spread through the CNS. Unlike brain lymphocytes from diseased wild-type mice, lymphocytes from perforin-deficient MRL mice showed no in vitro cytolytic activity towards target cells expressing the nucleoprotein of Borna disease virus. Taken together, these results demonstrate that CD8+ T cells mediate Borna disease independent of perforin. They further suggest that the pathogenic potential of CNS-infiltrating CD8+ T cells does not primarily reside in their lytic activity but rather in other functions. Twit Text FOAVip CD8+ T Lymphocytes Mediate Borna Disease Virus-Induced Immunopathology Independently of Perforin ????J Virol http://www.kidney.de/pget.php?&tw=1&pmid=11581414 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=11581414 #FOAvip English Wikipedia <ref>{{Cite pmid|11581414}}</ref> CD8+ T Lymphocytes Mediate Borna Disease Virus-Induced Immunopathology Independently of Perforin #MMPMID11581414 Hausmann J; Schamel K; Staeheli P J Virol 2001[Nov]; 75 (21): 10460-6 PMID11581414show ga Perforin-mediated lysis of target cells is the major antiviral effector mechanism of CD8+ T lymphocytes. We have analyzed the role of perforin in a mouse model for CD8+ T-cell-mediated central nervous system (CNS) immunopathology induced by Borna disease virus. When a defective perforin gene was introduced into the genetic background of the Borna disease-susceptible mouse strain MRL, the resulting perforin-deficient mice developed strong neurological disease in response to infection indistinguishable from that of their perforin-expressing littermates. The onset of disease was slightly delayed. Brains of diseased perforin-deficient mice showed similar amounts and a similar distribution of CD8+ T cells as wild-type animals. Perforin deficiency had no impact on the kinetics of viral spread through the CNS. Unlike brain lymphocytes from diseased wild-type mice, lymphocytes from perforin-deficient MRL mice showed no in vitro cytolytic activity towards target cells expressing the nucleoprotein of Borna disease virus. Taken together, these results demonstrate that CD8+ T cells mediate Borna disease independent of perforin. They further suggest that the pathogenic potential of CNS-infiltrating CD8+ T cells does not primarily reside in their lytic activity but rather in other functions. äCD8+ T Lymphocytes Mediate Borna Disease Virus-Induced Immunopathology(epmc).pdf DeepDyve Pubget Overpricing