Abstract
γδ T-cells play an important role in immune surveillance of acute myeloid leukemia (AML). The main circulating subtype expresses a Vγ9Vδ2 T-cell receptor and may be expanded <em>ex vivo</em> following aminobisphosphonate activation. While such protocols operate robustly in healthy donors, they are often inefficient using blood samples from patients with advanced malignancy.
Highlights
Introduction γδT-cells account for up to 3% of peripheral blood mononuclear cells (PBMC)
We explored the feasibility of zoledronic acid-mediated γδ T-cell expansion from patients with acute myeloid leukemia (AML)
Only a relatively small percentage of γδ T-cells could be identified in ficoll-separated PBMC derived from newly diagnosed AML patients
Summary
Introduction γδT-cells account for up to 3% of peripheral blood mononuclear cells (PBMC). Most express the Vγ9Vδ2 receptor, enabling their MHC-independent activation by phosphoantigen (PAg) intermediates of the mevalonate pathway [1]. Dysregulation of mevalonate pathway metabolism is prevalent in AML [2], accounting for the frequent sensitivity of leukemic cells to statins [3] or aminobisphosphonates (e.g. alendronic and zoledronic acid) [4]. Prolonged survival of AML patients after allogeneic hematopoietic stem cell transplantation (HSCT) correlates with enhanced γδ T-cell recovery. These cells may be expanded ex vivo following αβ T-cell-depleted haploidentical HSCT and exhibit potent cytolytic activity against primary AML cells. Infusion of haploidentical γδ T-cells followed by administration of zoledronic acid and IL-2 has induced complete remission
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