Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8721390 | Clinical Immunology | 2018 | 6 Pages |
Abstract
A high burden of CMV also drives accumulation of multifunctional terminally-differentiated αβ T-cells, a novel population of Vδ2 â 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.
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Authors
Shelley Waters, Emily Brook, Silvia Lee, Riwanti Estiasari, Ibnu Ariyanto, Patricia Price,