First, this is an observational study, and in the absence of a specific intervention targeting a necessary component of our model, our data are hypothesis-generating. Moreover, our observational cohorts are heterogeneous with respect to treatments received and other processes of care. Second, while we made every attempt to standardize BAL fluid volumes, the number of alveoli sampled and the return volume during both bronchoscopic and non-bronchoscopic BAL is variable. Hence, our observations are relative rather than quantitative. Third, our flow cytometry panels, while rigorous, were limited by the number of antibodies that could be used for high volume characterization of clinical samples. Fourth, our BAL samples were collected as part of clinical care; therefore, sicker patients were more likely to be sampled. Finally, while we made every effort to standardize care for patients with SARS-CoV-2 pneumonia in our ICU, some of our patients were enrolled in clinical trials of remdesivir or sarilumab, many patients received unproven therapies off label including hydroxychloroquine and tocilizumab, and our study largely preceded reports on the use of steroids in patients with severe SARS-CoV-2 pneumonia (Extended Data Table 1). Despite these limitations, our systems approach to understand SARS-CoV-2 pathobiology provides a model with testable predictions that can serve as a template for the design of targeted interventions in patients with severe disease.

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