The Longitudinal Immune Response to Coronavirus Disease 2019: Chasing the Cytokine Storm.

Publication Date

2020

Journal Title

Arthritis Rheumatol

Abstract

The clinical progression of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (COVID-19) to critical illness is associated with an exaggerated immune response, leading to magnified inflammation termed the "cytokine storm." This response is thought to contribute to the pathogenicity of severe COVID-19. There is an initial weak interferon response and macrophage activation that results in delayed neutrophil recruitment leading to impeded viral clearance. This causes prolonged immune stimulation and the release of proinflammatory cytokines. Elevated inflammatory markers in COVID-19 (i.e., D-dimer, C-reactive protein, lactate dehydrogenase, ferritin, and interleukin-6) are reminiscent of "cytokine storm" seen in severe hyperinflammatory macrophage disorders. The dysfunctional immune response in COVID-19 also includes lymphopenia, reduced T-cells, reduced natural killer cell maturation, and unmitigated plasmablast proliferation causing aberrant immunoglobulin G levels. The progression to severe disease is accompanied by endotheliopathy, immunothrombosis, and hypercoagulability. Thus, both parts of the immune system-innate and adaptive-play a significant role in the cytokine storm, multiorgan dysfunction, and coagulopathy. This review highlights the importance of understanding the immunological mechanisms of COVID-19 as they inform the clinical presentation and advise potential therapeutic targets.

Document Type

Article

Status

Faculty, Northwell Resident, SOM Student

Facility

School of Medicine; Northwell Health

Primary Department

Infectious Disease

Additional Departments

Rheumatology; General Internal Medicine; Pulmonary, Critical Care, and Sleep Medicine; General Pediatrics; COVID-19 Publications

PMID

32929876

DOI

10.1002/art.41526

For the public and Northwell Health campuses

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