| http://purl.uniprot.org/citations/15448711 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15448711 | http://www.w3.org/2000/01/rdf-schema#comment | "We previously showed that beta 2 microglobulin knockout mice depleted of NK cells by treatment with anti-asialoGM1 (beta2MKO/alphaAsGM1 mice) are resistant to sepsis caused by cecal ligation and puncture (CLP). beta2MKO mice possess multiple immunological defects including depletion of CD8+ T cells. This study was designed to determine the contribution of CD8+ T and NK cell deficiency to the resistance of beta2MKO/alphaAsGM1 mice to CLP-induced injury. beta2MKO/alphaAsGM1 mice and CD8 knockout mice treated with anti-asialoGM1 (CD8KO/alphaAsGM1 mice) survived significantly longer than wild-type mice following CLP. Improved long-term survival was also observed in wild-type mice rendered CD8+ T/NK cell-deficient by treatment with both anti-CD8alpha and anti-asialoGM1. Blood gas analysis and body temperature measurements showed that CD8+ T and NK cell-deficient mice have significantly reduced metabolic acidosis and less hypothermia compared to control mice at 18 h after CLP. CD8+ T/NK cell-deficient mice also showed an attenuated proinflammatory response as indicated by decreased expression of mRNAs for IL-1, IL-6 and MIP-2 in spleen and heart. IL-6, KC and MIP-2 levels in blood and peritoneal fluid were also significantly decreased CD8+ T/NK cell-deficient mice compared to controls. CD8+ T/NK cell-deficient mice exhibited decreased bacterial concentrations in blood, but not in peritoneal fluid or lung, compared to wild-type controls. These data show that mice depleted of CD8+ T and NK cells exhibit survival benefit, improved physiologic function and an attenuated proinflammatory response following CLP that is comparable to beta2M/alphaAsGM1 mice."xsd:string |
| http://purl.uniprot.org/citations/15448711 | http://purl.org/dc/terms/identifier | "doi:10.1038/labinvest.3700184"xsd:string |
| http://purl.uniprot.org/citations/15448711 | http://purl.uniprot.org/core/author | "Lin C.Y."xsd:string |
| http://purl.uniprot.org/citations/15448711 | http://purl.uniprot.org/core/author | "Sherwood E.R."xsd:string |
| http://purl.uniprot.org/citations/15448711 | http://purl.uniprot.org/core/author | "Enoh V.T."xsd:string |
| http://purl.uniprot.org/citations/15448711 | http://purl.uniprot.org/core/author | "Murphey E.D."xsd:string |
| http://purl.uniprot.org/citations/15448711 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/15448711 | http://purl.uniprot.org/core/name | "Lab Invest"xsd:string |
| http://purl.uniprot.org/citations/15448711 | http://purl.uniprot.org/core/pages | "1655-1665"xsd:string |
| http://purl.uniprot.org/citations/15448711 | http://purl.uniprot.org/core/title | "Mice depleted of CD8+ T and NK cells are resistant to injury caused by cecal ligation and puncture."xsd:string |
| http://purl.uniprot.org/citations/15448711 | http://purl.uniprot.org/core/volume | "84"xsd:string |
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