Article ID Journal Published Year Pages File Type
8721390 Clinical Immunology 2018 6 Pages PDF
Abstract
A high burden of CMV also drives accumulation of multifunctional terminally-differentiated αβ T-cells, a novel population of Vδ2 − γδ T-cells, and a population of CD56lo NK cells lacking a key regulatory molecule. An understanding of these “immunological footprints” of CMV may reveal how they collectively promote the “clinical footprints” of the virus. This is explored here in transplant recipients, HIV patients and healthy aging.
Related Topics
Life Sciences Immunology and Microbiology Immunology
Authors
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