Monocyte CD169 expression as a biomarker in the early diagnosis of COVID-19

Bedin, Anne‐Sophie; Makinson, Alain; Picot, Marie‐Christine; Mennechet, Frank; Malergue, Fabrice; Pisoni, Amandine; Nyiramigisha, Esperance; Montagnier, Lise; Bolloré, Karine; Debiesse, Ségolène; Morquin, David; Bourgoin, P; Veyrenche, Nicolas; Renault, Constance; Foulongne, Vincent; Bret, Caroline; Bourdin, Arnaud; Moing, Vincent Le; Perre, Philippe Van de; Tuaillon, Edouard

doi:10.1101/2020.06.28.20141556

Cited by 21 publications

(34 citation statements)

References 13 publications

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“…CD169 is a sialoadhesin involved in pathogen uptake, which is quickly induced in a type I IFN dependent manner on the surface of monocytes upon Epstein–Barr virus (EBV) or human immunodeficiency virus (HIV) infection (Rempel et al , 2008; Farina et al , 2017). Consistent with our findings, CD169 has been reported on circulating monocytes in COVID-19 patients (Bedin et al , 2020; Carissimo et al , 2020), while type I IFNs have been shown to be a hallmark of SARS-CoV-2 infection and an impaired type I IFN response has been linked with severe disease (Hadjadj et al , 2020; Wilk et al , 2020).…”

Section: Discussionsupporting

confidence: 91%

A distinct innate immune signature marks progression from mild to severe COVID-19

Chevrier

Zurbuchen

Cervia

et al. 2020

Preprint

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Coronavirus disease 2019 (COVID-19) manifests with a range of severities, but immune signatures of mild and severe disease are still not fully understood. Excessive inflammation has been postulated to be a major factor in the pathogenesis of severe COVID-19 and innate immune mechanisms are likely to be central in the inflammatory response. We used 40-plex mass cytometry and targeted serum proteomics to profile innate immune cell populations from peripheral blood of patients with mild or severe COVID-19 and healthy controls. Sampling at different stages of COVID-19 allowed us to reconstruct a pseudo-temporal trajectory of the innate immune response. Despite the expected patient heterogeneity, we identified consistent changes during the course of the infection. A rapid and early surge of CD169+ monocytes associated with an IFNy+MCP-2+ signature quickly followed symptom onset; at symptom onset, patients with mild and severe COVID-19 had a similar signature, but over the course of the disease, the differences between patients with mild and severe disease increased. Later in the disease course, we observed a more pronounced re-appearance of intermediate/non-classical monocytes and mounting systemic CCL3 and CCL4 levels in patients with severe disease. Our data provide new insights into the dynamic nature of the early inflammatory response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and identifies sustained pathological innate immune responses as a likely key mechanism in severe COVID-19, further supporting investigation of targeted anti-inflammatory interventions in severe COVID-19.

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Section: Discussionsupporting

confidence: 91%

A distinct innate immune signature marks progression from mild to severe COVID-19

Chevrier

Zurbuchen

Cervia

et al. 2020

Preprint

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“…Notably, IL-12p40 levels were inversely correlated with disease severity. Consistent with the observed increased levels of monocyte activation-associated biomarkers, and in agreement with recent reports (26,27), peripheral blood monocytes of COVID-19 patients exhibited extensive vacuolization (Supplementary Figure 5A), and the MFIs of CD169, and of CD63, CD11b and b558 were greater in peripheral blood CD14 + monocytes of COVID-19 patients (n = 2) relative to HV (Supplementary Figure 6).…”

Section: Monocyte/macrophage Activation-associated Biomarkers Are Marsupporting

confidence: 91%

An immune-based biomarker signature is associated with mortality in COVID-19 patients

Abers¹,

Delmonte²,

Ricotta³

et al. 2021

JCI Insight

298

301

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“…Even if local tissue macrophages do not express ACE2 receptors and are not directly infected, they play a role in inflammatory cytokine responses to infected cells through surface, endosomal and cytosolic receptors and secretion of IL-1 family members [52] and antiviral interferons (IFNs). Monocytes, dendritic cells and tissue macrophages can bind virus through lectin-like receptors such as CD169 [53] , for transport to regional lymph nodes. Delivery of virus droplets to the lower respiratory tract leads to infection of ACE2+ alveolar epithelium and capillary endothelium.…”

Section: Covid-19 Infectionmentioning

confidence: 99%

Monocyte activation in systemic Covid-19 infection: Assay and rationale

et al. 2020

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Mononuclear phagocytes are a widely distributed family of cells contributing to innate and adaptive immunity. Circulating monocytes and tissue macrophages participate in all stages of SARS COVID-19. They contribute to comorbidities predisposing to clinical infection, virus resistance and dissemination, and to host factors that determine disease severity, recovery and sequelae. Assays are available to detect viral infection and antibody responses, but no adequate tests have been developed to measure the activation level of monocytes and tissue macrophages, and the risk of progression to a fatal hyperinflammatory syndrome. Blood monocytes provide a window on the systemic immune response, from production to tissue recruitment, reflecting the impact of infection on the host. Ready availability of blood makes it possible to monitor severity and the risk of potentially lethal complications, by developing tests to assess the status of monocyte activation and its potential for further inflammatory dysregulation after recruitment to tissues and during recovery.

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Monocyte CD169 expression as a biomarker in the early diagnosis of COVID-19

Cited by 21 publications

References 13 publications

A distinct innate immune signature marks progression from mild to severe COVID-19

A distinct innate immune signature marks progression from mild to severe COVID-19

An immune-based biomarker signature is associated with mortality in COVID-19 patients

Monocyte activation in systemic Covid-19 infection: Assay and rationale

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