Abstract
BackgroundHuman Ebola infection is characterized by a paralysis of the immune system. A signature of αβ T cells in fatal Ebola infection has been recently proposed, while the involvement of innate immune cells in the protection/pathogenesis of Ebola infection is unknown. Aim of this study was to analyze γδ T and NK cells in patients from the Ebola outbreak of 2014–2015 occurred in West Africa, and to assess their association with the clinical outcome.Methodology/Principal findingsNineteen Ebola-infected patients were enrolled at the time of admission to the Ebola Treatment Centre in Guinea. Patients were divided in two groups on the basis of the clinical outcome. The analysis was performed by using multiparametric flow cytometry established by the European Mobile Laboratory in the field. A low frequency of Vδ2 T-cells was observed during Ebola infection, independently from the clinical outcome. Moreover, Vδ2 T-cells from Ebola patients massively expressed CD95 apoptotic marker, suggesting the involvement of apoptotic mechanisms in Vδ2 T-cell loss. Interestingly, Vδ2 T-cells from survivors expressed an effector phenotype and presented a lower expression of the CTLA-4 exhaustion marker than fatalities, suggesting a role of effector Vδ2 T-cells in the protection. Furthermore, patients with fatal Ebola infection were characterized by a lower NK cell frequency than patients with non fatal infection. In particular, both CD56bright and CD56dim NK frequency were very low both in fatal and non fatal infections, while a higher frequency of CD56neg NK cells was associated to non-fatal infections. Finally, NK activation and expression of NKp46 and CD158a were independent from clinical outcome.Conclusions/SignificancesAltogether, the data suggest that both effector Vδ2 T-cells and NK cells may play a role in the complex network of protective response to EBOV infection. Further studies are required to characterize the protective effector functions of Vδ2 and NK cells.
Highlights
Ebola virus (EBOV) is a member of the Filoviridae family, which is filamentous, negativestranded RNA viruses that is known to cause severe human disease [1]
Our results show that both effector Vδ2 T-cells and NK cells were associated with survival, suggesting their involvement in the complex network of protective response to EBOV infection
When compared to HD, a lower frequency of Vδ2 T-cells was observed during acute EBOV infection, independently from the clinical outcome (Fig 1A, p
Summary
Ebola virus (EBOV) is a member of the Filoviridae family, which is filamentous, negativestranded RNA viruses that is known to cause severe human disease [1]. The innate immune reaction is characterized by a cytokine storm, with secretion of numerous pro-inflammatory cytokines, which induce a huge number of contradictory signals, and impair the immune cells, as well as other tissues [2,3]. A high expression of the T cell inhibitory molecules cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death-1 (PD-1) on CD8 and CD4 T cells was associated to fatal infections, and was correlated with elevated inflammatory markers and high viral load. These data confirm that a deregulation of T-cell response represents a key component of EBOV pathology [8]. Aim of this study was to analyze γδ T and NK cells in patients from the Ebola outbreak of 2014– 2015 occurred in West Africa, and to assess their association with the clinical outcome
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