Antigen-specific γδ T cells contribute to cytomegalovirus control after stem cell transplantation

Despite prophylactic or preemptive pharmacological treatment, cytomegalovirus (CMV) seropositivity and reactivation of remain associated with increased morbidity and mortality after allogeneic hematopoietic stem cell transplantation (alloHSCT) 1, 2. In healthy individuals, control of latent CMV infection depends on several layers of immune cells, in particular the lymphocyte lineages natural killer (NK) cells, αβ T cells, and γδ T cells. As recently discussed elsewhere 3, 4, rapidly expanding donor NK cells support the control of CMV reactivation early after alloHSCT and may at the same time contribute to graft-versus-leukemia reactions. In contrast, the reconstitution of potent antiviral CD4+ and CD8+ αβ T cells takes several weeks to months and also depends on the CMV serostatus of the alloHSCT donor and leaves the patients susceptible to CMV reactivation or even CMV disease [5].

In this review, we report interdisciplinary work performed within a DFG-funded research consortium CRC900 investigating microbial persistence and its control in chronic infections. We focus on studies investigating the activation of γδ T cells in the context of CMV reactivation after alloHSCT, their potential γδ T cell receptors (TCR) ligands, and discuss their contribution to CMV control.

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