1 results match your criteria: "Bethesda eCollaborative Clinical Research Branch[Affiliation]"

HIV immune activation drives increased Eomes expression in memory CD8 T cells in association with transcriptional downregulation of CD127.

AIDS

July 2013

aCMRS/Laboratory of Immunoregulation, NIAID bExperimental Immunology Branch, NCI, NIH, Bethesda cLaboratory of Molecular Immunoregulation, NCI, NIH, Frederick dBiostatistics Research Branch, NIAID, NIH, Bethesda eCollaborative Clinical Research Branch, NIAID, NIH, Frederick, Maryland, USA.

Background: During HIV infection distinct mechanisms drive immune activation of the CD4 and CD8 T cells leading to CD4 T-cell depletion and expansion of the CD8 T-cell pool. This immune activation is polyclonal and extends beyond HIV-specific T cells. One consequence of this immune activation is a profound decrease in IL-7Rα (CD127) expression on memory CD8 T cells.

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