SARS‐CoV2 pneumonia recovery is linked to expansion of innate lymphoid cells type 2 expressing CCR10

• Published in: European Journal of Immunology 2021-12, Vol.51 (12), p.3194-3201
• Main Authors: Gomes, André M. C., Farias, Guilherme B., Dias‐Silva, Manuel, Laia, Joel, Trombetta, Amelia C., Godinho‐Santos, Ana, Rosmaninho, Pedro, Santos, Diana F., Conceição, Carolina M., Costa‐Reis, Renato, Adão‐Serrano, Maria, Mota, Catarina, Almeida, Afonso R. M., Sousa, Ana E., Fernandes, Susana M.
• Format: Article
• Language: English
• Subjects: Adult; Aged; Antigens, Neoplasm - metabolism; Biomarkers - metabolism; CCR10; Cell Proliferation; COVID-19; COVID-19 - immunology; Cytokines - metabolism; Female; Homeostasis; Humans; Immunity to infection; Immunity, Innate; Inflammation; Innate lymphoid cells; Lung - pathology; Lung recovery; Lymphocytes; Lymphocytes - immunology; Lymphoid cells; Male; Middle Aged; Mitogen-Activated Protein Kinases - metabolism; Mucosa; Oxygenation; Pandemics; Patients; Phenotypes; Pneumonia; Pneumonia, Viral - immunology; Receptors, CCR10 - metabolism; Recovery of Function; Respiratory failure; Respiratory function; SARS-CoV-2 - physiology; SARS‐CoV2; Severe acute respiratory syndrome coronavirus 2; Short Communication|Clinical; Th2 Cells - immunology; Up-Regulation
• ISSN: 0014-2980; 1521-4141; 1521-4141
• DOI: 10.1002/eji.202149311

Accelerate lung repair in SARS‐CoV‐2 pneumonia is essential for pandemic handling. Innate lymphoid cells (ILCs) are likely players, given their role in mucosal protection and tissue homeostasis. We studied ILC subpopulations at two time points in a cohort of patients admitted in the hospital due to SARS‐CoV‐2 infection. COVID‐19 patients with moderate/severe respiratory failure featured profound depletion of circulating ILCs at hospital admission, in agreement with overall lymphocyte depletion. However, ILCs recovered in direct correlation with lung function improvement as measured by oxygenation index and in negative association with inflammatory and lung/endothelial damage markers like RAGE. While both ILC1 and ILC2 expanded, ILC2 showed the most striking phenotype changes, with CCR10 upregulation in strong correlation with these parameters. Overall, CCR10+ ILC2 emerge as relevant contributors to SARS‐CoV‐2 pneumonia recovery. Moderate to severe COVID‐19 is associated with an overall decrease in all innate lymphoid cells’ subsets in parallel with the well‐known lymphopenia. We report, in association with the oxygenation improvement, a significant expansion of ILC1, irrespectively of CD161 expression, and of CCR10 expressing ILC2, suggesting their involvement in lung regeneration.