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10.2353/ajpath.2009.080897 http://scihub22266oqcxt.onion/10.2353/ajpath.2009.080897 C2671268!2671268!19359516     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 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       Am+J+Pathol 2009 ; 174 (5): 1799-807 Nephropedia Template TP {{tp|p=19359516|t=2009. Interferon-? Prevents Death of Bystander Neurons during CD8 T Cell Responses in the Brain |pdf=|usr=}}{{19359516}} gab.com Text Interferon- Prevents Death of Bystander Neurons during CD8 T Cell Responses in the Brain JO: Am J Pathol http://www.kidney.de/pget.php?&tw=1&pmid=19359516 #FOAvip T cells restricted to neurotropic viruses are potentially harmful as their activity may result in the destruction of neurons. In the Borna disease virus (BDV) model, antiviral CD8 T cells entering the brain of infected mice cause neurological disease but no substantial loss of neurons unless the animals lack interferon-? (IFN-?). We show here that glutamate receptor antagonists failed to prevent BDV-induced neuronal loss in IFN-?-deficient mice, suggesting that excitotoxicity resulting from glutamate receptor overstimulation is an unlikely explanation for the neuronal damage. Experiments with IFN-?-deficient mice lacking eosinophils indicated that these cells, which specifically accumulate in the infected brains of IFN-?-deficient mice, are not responsible for CA1 neuronal death. Interestingly, BDV-induced damage of CA1 neurons was reduced significantly in IFN-?-deficient mice lacking perforin, suggesting a key role for CD8 T cells in this pathological process. Specific death of hippocampal CA1 neurons could be triggered by adoptive transfer of BDV-specific CD8 T cells from IFN-?-deficient mice into uninfected mice that express transgene-encoded BDV antigen at high level in astrocytes. These results indicate that attack by CD8 T cells that cause the death of CA1 neurons might be directed toward regional astrocytes and that IFN-? protects vulnerable CA1 neurons from collateral damage resulting from exposure to potentially toxic substances generated as a result of CD8 T cell-mediated impairment of astrocyte function. Twit Text FOAVip Interferon- Prevents Death of Bystander Neurons during CD8 T Cell Responses in the Brain ????Am J Pathol http://www.kidney.de/pget.php?&tw=1&pmid=19359516 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19359516 #FOAvip English Wikipedia <ref>{{Cite pmid|19359516}}</ref> Interferon-? Prevents Death of Bystander Neurons during CD8 T Cell Responses in the Brain #MMPMID19359516 Richter K; Hausmann J; Staeheli P Am J Pathol 2009[May]; 174 (5): 1799-807 PMID19359516show ga T cells restricted to neurotropic viruses are potentially harmful as their activity may result in the destruction of neurons. In the Borna disease virus (BDV) model, antiviral CD8 T cells entering the brain of infected mice cause neurological disease but no substantial loss of neurons unless the animals lack interferon-? (IFN-?). We show here that glutamate receptor antagonists failed to prevent BDV-induced neuronal loss in IFN-?-deficient mice, suggesting that excitotoxicity resulting from glutamate receptor overstimulation is an unlikely explanation for the neuronal damage. Experiments with IFN-?-deficient mice lacking eosinophils indicated that these cells, which specifically accumulate in the infected brains of IFN-?-deficient mice, are not responsible for CA1 neuronal death. Interestingly, BDV-induced damage of CA1 neurons was reduced significantly in IFN-?-deficient mice lacking perforin, suggesting a key role for CD8 T cells in this pathological process. Specific death of hippocampal CA1 neurons could be triggered by adoptive transfer of BDV-specific CD8 T cells from IFN-?-deficient mice into uninfected mice that express transgene-encoded BDV antigen at high level in astrocytes. These results indicate that attack by CD8 T cells that cause the death of CA1 neurons might be directed toward regional astrocytes and that IFN-? protects vulnerable CA1 neurons from collateral damage resulting from exposure to potentially toxic substances generated as a result of CD8 T cell-mediated impairment of astrocyte function. äInterferon-? Prevents Death of Bystander Neurons during CD8 T Cell Res(epmc).pdf DeepDyve Pubget Overpricing