<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Buchlis, G</style></author><author><style face="normal" font="default" size="100%">Odorizzi, P</style></author><author><style face="normal" font="default" size="100%">Soto, PC</style></author><author><style face="normal" font="default" size="100%">Pearce, OM</style></author><author><style face="normal" font="default" size="100%">Hui, DJ</style></author><author><style face="normal" font="default" size="100%">Jordan, MS</style></author><author><style face="normal" font="default" size="100%">Ajit Varki</style></author><author><style face="normal" font="default" size="100%">Wherry, EJ</style></author><author><style face="normal" font="default" size="100%">High, KA</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Enhanced T cell function in a mouse model of human glycosylation</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of Immunology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">CD4-Positive T-Lymphocytes/immunology/metabolism/virology</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Proliferation</style></keyword><keyword><style  face="normal" font="default" size="100%">Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Cultured</style></keyword><keyword><style  face="normal" font="default" size="100%">Dependovirus/genetics/immunology/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Glycosylation</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Lymphocyte Activation/*genetics/*immunology</style></keyword><keyword><style  face="normal" font="default" size="100%">Lymphocytic choriomeningitis virus/ge</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Jul 1</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691298/</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">1</style></number><edition><style face="normal" font="default" size="100%">2013/05/28</style></edition><volume><style face="normal" font="default" size="100%">191</style></volume><pages><style face="normal" font="default" size="100%">228-37</style></pages><isbn><style face="normal" font="default" size="100%">1550-6606 (Electronic)00</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Clinical evidence for a more active immune response in humans compared with our closest hominid relative, the chimpanzee, includes the progression of HIV infection to AIDS, hepatitis B- and C-related inflammation, autoimmunity, and unwanted harmful immune responses to viral gene transfer vectors. Humans have a unique mutation of the enzyme CMP-N-acetylneuraminic acid hydroxylase (CMAH), causing loss of expression of the sialic acid Neu5Gc. This mutation, occurring 2 million years ago, likely altered the expression and function of ITIM-bearing inhibitory receptors (Siglecs) that bind sialic acids. Previous work showed that human T cells proliferate faster than chimpanzee T cells upon equivalent stimulation. In this article, we report that Cmah(-/-) mouse T cells proliferate faster and have greater expression of activation markers than wild-type mouse T cells. Metabolically reintroducing Neu5Gc diminishes the proliferation and activation of both human and murine Cmah(-/-) T cells. Importantly, Cmah(-/-) mice mount greater T cell responses to an adenovirus encoding an adeno-associated virus capsid transgene. Upon lymphocytic choriomeningitis virus infection, Cmah(-/-) mice make more lymphocytic choriomeningitis virus-specific T cells than WT mice, and these T cells are more polyfunctional. Therefore, a uniquely human glycosylation mutation, modeled in mice, leads to a more proliferative and active T cell population. These findings in a human-like mouse model have implications for understanding the hyperimmune responses that characterize some human diseases.&lt;/p&gt;
</style></abstract><work-type><style face="normal" font="default" size="100%">Research Support, N.I.H., ExtramuralResearch Support, Non-U.S. Gov&#039;t</style></work-type><accession-num><style face="normal" font="default" size="100%">23709682</style></accession-num><notes><style face="normal" font="default" size="100%">&lt;p&gt;J Immunol. 2013 Jul 1;191(1):228-37. doi: 10.4049/jimmunol.1202905. Epub 2013 May 24.&lt;/p&gt;
</style></notes><custom2><style face="normal" font="default" size="100%">3691298</style></custom2><auth-address><style face="normal" font="default" size="100%">University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.</style></auth-address></record></records></xml>