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dc.contributor.authorMichael A. Elleren_US
dc.contributor.authorKim G. Blomen_US
dc.contributor.authorVeronica D. Gonzalezen_US
dc.contributor.authorLeigh Anne Elleren_US
dc.contributor.authorProssy Naluyimaen_US
dc.contributor.authorOliver Laeyendeckeren_US
dc.contributor.authorThomas C. Quinnen_US
dc.contributor.authorNoah Kiwanukaen_US
dc.contributor.authorDavid Serwaddaen_US
dc.contributor.authorNelson K. Sewankamboen_US
dc.contributor.authorBoonrat Tasseneetrithepen_US
dc.contributor.authorMaria J. Waweren_US
dc.contributor.authorRonald H. Grayen_US
dc.contributor.authorMary A. Marovichen_US
dc.contributor.authorNelson L. Michaelen_US
dc.contributor.authorMark S. de Souzaen_US
dc.contributor.authorFred Wabwire-Mangenen_US
dc.contributor.authorMerlin L. Robben_US
dc.contributor.authorJeffrey R. Currieren_US
dc.contributor.authorJohan K. Sandbergen_US
dc.contributor.otherMakerere Universityen_US
dc.contributor.otherU.S. Military HIV Research Programen_US
dc.contributor.otherKarolinska University Hospitalen_US
dc.contributor.otherNational Institute of Allergy and Infectious Diseasesen_US
dc.contributor.otherThe Johns Hopkins School of Medicineen_US
dc.contributor.otherUganda Virus Research Instituten_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherColumbia University Medical Centeren_US
dc.contributor.otherJohns Hopkins Universityen_US
dc.contributor.otherArmed Forces Research Institute of Medical Sciences, Thailanden_US
dc.date.accessioned2018-05-03T07:56:39Z-
dc.date.available2018-05-03T07:56:39Z-
dc.date.issued2011-05-02en_US
dc.identifier.citationPLoS ONE. Vol.6, No.4 (2011)en_US
dc.identifier.issn19326203en_US
dc.identifier.other2-s2.0-79955384228en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=79955384228&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/11321-
dc.description.abstractHIV-1 disease progression is associated with persistent immune activation. However, the nature of this association is incompletely understood. Here, we investigated immune activation in the CD4 T cell compartment of chronically HIV-1 infected individuals from Rakai, Uganda. Levels of CD4 T cell activation, assessed as co-expression of PD-1, CD38 and HLA-DR, correlated directly to viral load and inversely to CD4 count. Deeper characterization of these cells indicated an effector memory phenotype with relatively frequent expression of Ki67 despite their PD-1 expression, and levels of these cells were inversely associated with FoxP3+ regulatory T cells. We therefore use the term deregulated effector memory (DEM) cells to describe them. CD4 T cells with a DEM phenotype could be generated by antigen stimulation of recall responses in vitro. Responses against HIV-1 and CMV antigens were enriched among the DEM CD4 T cells in patients, and the diverse Vβ repertoire of DEM CD4 T cells suggested they include diverse antigen-specificities. Furthermore, the levels of DEM CD4 T cells correlated directly to soluble CD14 (sCD14) and IL-6, markers of innate immune activation, in plasma. The size of the activated DEM CD4 T cell subset was predictive of the rate of disease progression, whereas IL-6 was only weakly predictive and sCD14 was not predictive. Taken together, these results are consistent with a model where systemic innate immune activation and chronic antigen stimulation of adaptive T cell responses both play important roles in driving pathological CD4 T cell immune activation in HIV-1 disease.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=79955384228&origin=inwarden_US
dc.subjectAgricultural and Biological Sciencesen_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleInnate and adaptive immune responses both contribute to pathological cd4 t cell activation in hiv-1 infected ugandansen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.1371/journal.pone.0018779en_US
Appears in Collections:Scopus 2011-2015

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