Background: Normally, regulatory T cells (also known as T regulatory cells or Tregs) migrate into inflamed tissues, dampening inflammatory responses and hastening tissue repair (1). Patients with coronavirus disease 2019 (COVID-19) and acute respiratory distress syndrome (ARDS) have protracted hospitalizations characterized by excessive systemic inflammation (cytokine storm) and delayed lung repair, which is partly due to reduced or defective Tregs (2).

Objective: To describe outcomes in 2 patients with COVID-19 and ARDS who were treated with Tregs.

Case Reports: The first patient was a 69-year-old man with autism who was hospitalized from his nursing home with COVID-19–induced fever and dyspnea 1 week after initial symptom onset. Despite 5 days of receiving hydroxychloroquine and broad-spectrum antimicrobial agents, he progressed to ARDS and received tocilizumab on day 7 and mechanical ventilation beginning on day 8. Renal failure and shock developed, requiring continuous, venovenous hemofiltration and vasopressors. Refractory hypoxemia required prone positioning, neuromuscular paralysis, inhaled nitric oxide, and FI O 2 greater than 70%. We administered compassionate use, cryopreserved, allogeneic Tregs derived from cord blood (CB) and expanded ex vivo (Cellenkos) at 1× 10 8 cells per dose intravenously on days 13 and 17. By day 17, he had returned to supine positioning, paralytics were withdrawn, inhaled nitric oxide was weaned to zero, FI O 2 was decreased to 50%, vasopressors were withdrawn, and inflammatory markers were reduced (Table 1). He was extubated on day 22. On day 25, he required a tracheostomy. He is currently receiving care in a weaning facility.