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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\u201019 (e.g.,\n                    <jats:sc>d<\/jats:sc>\n                    \u2010dimer, C\u2010reactive protein, lactate dehydrogenase, ferritin, and interleukin\u20106) are reminiscent of the cytokine storm seen in severe hyperinflammatory macrophage disorders. The dysfunctional immune response in COVID\u201019 also includes lymphopenia, reduced T cells, reduced natural killer cell maturation, and unmitigated plasmablast proliferation causing aberrant IgG levels. The progression to severe disease is accompanied by endotheliopathy, immunothrombosis, and hypercoagulability. Thus, both parts of the immune system\u2014innate and adaptive\u2014play a significant role in the cytokine storm, multiorgan dysfunction, and coagulopathy. This review highlights the importance of understanding the immunologic mechanisms of COVID\u201019 as they inform the clinical presentation and advise potential therapeutic targets.\n                  <\/jats:p>","DOI":"10.1002\/art.41526","type":"journal-article","created":{"date-parts":[[2020,9,21]],"date-time":"2020-09-21T03:25:25Z","timestamp":1600658725000},"page":"23-35","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":55,"title":["The Longitudinal Immune Response to Coronavirus Disease 2019: Chasing the Cytokine Storm"],"prefix":"10.1002","volume":"73","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6924-9870","authenticated-orcid":false,"given":"Alice S.","family":"Chau","sequence":"first","affiliation":[{"name":"University of Washington Center for Immunity and Immunotherapies and Seattle Children\u2019s Research Institute  Seattle Washington United 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