Platelet Induced Functional Alteration of CD4+ and CD8+ T Cells in HNSCC

Polasky, Christina; Wendt, Franziska; Pries, Ralph; Wollenberg, Barbara

doi:10.3390/ijms21207507

Cited by 16 publications

(11 citation statements)

References 69 publications

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“…Upon activation, platelets can secrete numerous soluble inflammatory mediators and/or bind to leukocytes, thus exerting an immune effect (Rachidi et al, 2017;Zamora et al, 2017;Polasky et al, 2020;Zimmer et al, 2020). In the present study, transwell assays confirmed that the regulation of IFN-g production in T cells…”

Section: Discussionsupporting

confidence: 81%

Platelets correlate with false negative T-SPOT.TB results by inhibiting interferon-γ production in T cells via degranulation

Rao

Rao²,

Guo³

et al. 2022

Front. Cell. Infect. Microbiol.

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BackgroundT-SPOT.TB (T-SPOT) is widely used for the detection of Mycobacterium tuberculosis infection by detecting interferon-gamma (IFN-γ) release in T lymphocytes. This assay is performed on peripheral blood mononuclear cells (PBMCs) separated by Ficoll density gradient centrifugation, which often contain some residual platelets. Here, we investigated the impact of platelets on T-SPOT assay and related mechanisms.MethodsThe correlation between platelet count, platelet-to-lymphocyte ratio (PLR), and the IFN-γ secreting T cells (ISCs) in positive control wells of T-SPOT assay were retrospectively analyzed. T-SPOT assay was performed with un-treated PBMCs, platelets-removed PBMCs, and platelets-enriched PBMCs to confirm the impact of platelets on T-SPOT assay. The activation of platelets and their impact on IFN-γ production in T cells were detected by flow cytometry (FCM). Platelets and T cells were cultured in a mixed culture system and co-culture system respectively, followed by detection of the frequencies of IFN-γ-producing T cells and the levels of intracellular IFN-γ in T cells by FCM. Moreover, the effect of platelet releasate on the T-SPOT assay was evaluated.ResultsThe ISCs in positive control wells of the T-SPOT assay showed a significant decrease with the increase in platelet count. The PLR of the peripheral blood were negatively correlated with the ISCs in positive control wells of the T-SPOT assay. Removal or enrichment of platelets significantly increased or decreased the ISCs and the positive rate of T-SPOT. Inhibition of platelet activation significantly increased the ISCs of T-SPOT. The frequencies of IFN-γ-producing T cells in PBMCs and the levels of intracellular IFN-γ were significantly reduced by the addition of platelets, both in the mixed culture system and the co-culture system. Platelet releasate upon thrombin activation significantly decreased the ISCs of T-SPOT.ConclusionsPlatelets correlate with negative T-SPOT results by inhibiting IFN-γ production in T cells via degranulation.

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Section: Discussionsupporting

confidence: 81%

Platelets correlate with false negative T-SPOT.TB results by inhibiting interferon-γ production in T cells via degranulation

Rao

Rao²,

Guo³

et al. 2022

Front. Cell. Infect. Microbiol.

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“…Activated platelets may associate with T cells in the blood of HIV‐infected individuals (Green et al., 2015 ) and link the coagulation and inflammatory cascade with T cells. In vitro, platelets can inhibit proliferation, cytokine production and PD1 expression of T cells (Polasky et al., 2020 ). Since PMPs derive from platelets, they may also have similar functions as their 'parent’‐platelets.…”

Section: Discussionmentioning

confidence: 99%

Binding of phosphatidylserine‐positive microparticles by PBMCs classifies disease severity in COVID‐19 patients

Rausch¹,

Lutz²,

Schifferer

et al. 2021

J of Extracellular Vesicle

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Infection with SARS‐CoV‐2 is associated with thromboinflammation, involving thrombotic and inflammatory responses, in many COVID‐19 patients. In addition, immune dysfunction occurs in patients characterised by T cell exhaustion and severe lymphopenia. We investigated the distribution of phosphatidylserine (PS), a marker of dying cells, activated platelets and platelet‐derived microparticles (PMP), during the clinical course of COVID‐19. We found an unexpectedly high amount of blood cells loaded with PS + PMPs for weeks after the initial COVID‐19 diagnosis. Elevated frequencies of PS + PMP + PBMCs correlated strongly with increasing disease severity. As a marker, PS outperformed established laboratory markers for inflammation, leucocyte composition and coagulation, currently used for COVID‐19 clinical scoring. PS + PMPs preferentially bound to CD8 + T cells with gene expression signatures of proliferating effector rather than memory T cells. As PS + PMPs carried programmed death‐ligand 1 (PD‐L1), they may affect T cell expansion or function. Our data provide a novel marker for disease severity and show that PS, which can trigger the blood coagulation cascade, the complement system, and inflammation, resides on activated immune cells. Therefore, PS may serve as a beacon to attract thromboinflammatory processes towards lymphocytes and cause immune dysfunction in COVID‐19.

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“…Activated platelets may associate with T cells in the blood of HIV-infected individuals 68 and link the coagulation and inflammatory cascade with T cells. In vitro , platelets can inhibit proliferation, cytokine production, and PD1 expression of T cells 69 . Since PMPs derive from platelets, they may also have similar functions as their ‘parent’-platelets.…”

Section: Discussionmentioning

confidence: 99%

“…In vitro, platelets can inhibit proliferation, cytokine production, and PD1 expression of T cells 69 . Since PMPs derive from platelets, they may also have similar functions as their 'parent'platelets.…”

Section: Pmps Carry Markers Of Activated Plateletsmentioning

confidence: 99%

Binding of phosphatidylserine-positive microparticles by PBMCs classifies disease severity in COVID-19 patients

Rausch¹,

Lutz²,

Schifferer

et al. 2021

Preprint

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Infection with SARS-CoV-2 is associated with thromboinflammation, involving thrombotic and inflammatory responses, in many COVID-19 patients. In addition, immune dysfunction occurs in patients characterized by T cell exhaustion and severe lymphopenia. We investigated the distribution of phosphatidylserine (PS), a marker of dying cells, activated platelets, and platelet-derived microparticles (PMP), during the clinical course of COVID-19. We found an unexpectedly high amount of blood cells loaded with PS+ PMPs for weeks after the initial COVID-19 diagnosis. Elevated frequencies of PS+PMP+ PBMCs correlated strongly with increasing disease severity. As a marker, PS outperformed established laboratory markers for inflammation, leucocyte composition, and coagulation, currently used for COVID-19 clinical outcome prognosis. PS+ PMPs preferentially bound to CD8+ T cells with gene expression signatures of proliferating effector rather than memory T cells. As PS+ PMPs carried programmed death-ligand 1 (PD-L1), they may affect T cell expansion or function. Our data provide a novel marker for disease severity and show that PS, which can trigger the blood coagulation cascade, the complement system, and inflammation, resides on activated immune cells. Therefore, PS may serve as a beacon to attract thromboinflammatory processes toward lymphocytes and cause immune dysfunction in COVID-19.

show abstract

Platelet Induced Functional Alteration of CD4+ and CD8+ T Cells in HNSCC

Cited by 16 publications

References 69 publications

Platelets correlate with false negative T-SPOT.TB results by inhibiting interferon-γ production in T cells via degranulation

Platelets correlate with false negative T-SPOT.TB results by inhibiting interferon-γ production in T cells via degranulation

Binding of phosphatidylserine‐positive microparticles by PBMCs classifies disease severity in COVID‐19 patients

Binding of phosphatidylserine-positive microparticles by PBMCs classifies disease severity in COVID-19 patients

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