期刊
IMMUNITY
卷 54, 期 6, 页码 1257-+出版社
CELL PRESS
DOI: 10.1016/j.immuni.2021.05.010
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资金
- CVC Capital Partners, the Evelyn Trust [20/75]
- Addenbrooke's Charitable Trust, Cambridge University Hospitals [12/20A]
- NIHR Cambridge Biomedical Research Centre
- UKRI/NIHR through the UK Coronavirus Immunology Consortium (UK-CIC)
- Wellcome Investigator Award [200871/Z/16/Z]
- Wellcome Senior Clinical Research Fellowship [108070/Z/15/Z]
- Wellcome [207498/Z/17/Z]
- Fondation Botnar
- MRC (CSF) [MR/P008801/1]
- NHSBT [WPA15-02]
- Addenbrooke's Charitable Trust [900239]
- Wellcome Senior Fellowship
- Wellcome Trust Principal Research Fellowship [084957/Z/08/Z]
- MRC [MR/V011561/1]
- Spinnaker Healthcare Research Trust
- McCusker Foundation, Australian National Phenome Centre
- Jacquot Research Entry Scholarship of the Royal Australasian College of Physicians Foundation
- MRC Clinical Infrastructure Award
- Wellcome Trust [200871/Z/16/Z, 207498/Z/17/Z] Funding Source: Wellcome Trust
- MRC [MR/V011561/1, MR/S036113/1, MR/W014556/1] Funding Source: UKRI
The kinetics of immune changes in COVID-19 across different severity groups show that early bystander CD8(+) T cell immune response is prominent in asymptomatic or mild diseases, while severe cases have persistent cellular abnormalities and immune defects, which may increase clinical risks.
The kinetics of the immune changes in COVID-19 across severity groups have not been rigorously assessed. Using immunophenotyping, RNA sequencing, and serum cytokine analysis, we analyzed serial samples from 207 SARS-CoV2-infected individuals with a range of disease severities over 12 weeks from symptom onset. An early robust bystander CD8(+) T cell immune response, without systemic inflammation, characterized asymptomatic or mild disease. Hospitalized individuals had delayed bystander responses and systemic inflammation that was already evident near symptom onset, indicating that immunopathology may be inevitable in some individuals. Viral load did not correlate with this early pathological response but did correlate with subsequent disease severity. Immune recovery is complex, with profound persistent cellular abnormalities in severe disease correlating with altered inflammatory responses, with signatures associated with increased oxidative phosphorylation replacing those driven by cytokines tumor necrosis factor (TNF) and interleukin (IL)-6. These late immunometabolic and immune defects may have clinical implications.
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