
| 10.4049/jimmunol.2001325
http://scihub22266oqcxt.onion/10.4049/jimmunol.2001325
 33846224!�!33846224
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J+Immunol 2021 ; 206 (9): 2146-2159 Nephropedia Template TP
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Longitudinal Peripheral Blood Transcriptional Analysis Reveals Molecular Signatures of Disease Progression in COVID-19 Patients #MMPMID33846224Yan Q; Li P; Ye X; Huang X; Feng B; Ji T; Chen Z; Li F; Zhang Y; Luo K; Chen F; Mo X; Wang J; Feng L; Hu F; Lei C; Qu L; Chen LJ Immunol 2021[May]; 206 (9): 2146-2159 PMID33846224show ga
Coronavirus disease 2019 (COVID-19) is caused by a novel coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), with some patients developing severe illness or even death. Disease severity has been associated with increased levels of proinflammatory cytokines and lymphopenia. To elucidate the atlas of peripheral immune response and pathways that might lead to immunopathology during COVID-19 disease course, we performed a peripheral blood RNA sequencing analysis of the same patient's samples collected from symptom onset to full recovery. We found that PBMCs at different disease stages exhibited unique transcriptome characteristics. We observed that SARS-CoV-2 infection caused excessive release of inflammatory cytokines and lipid mediators as well as an aberrant increase of low-density neutrophils. Further analysis revealed an increased expression of RNA sensors and robust IFN-stimulated genes expression but a repressed type I IFN production. SARS-CoV-2 infection activated T and B cell responses during the early onset but resulted in transient adaptive immunosuppression during severe disease state. Activation of apoptotic pathways and functional exhaustion may contribute to the reduction of lymphocytes and dysfunction of adaptive immunity, whereas increase in IL2, IL7, and IL15 may facilitate the recovery of the number and function of lymphocytes. Our study provides comprehensive transcriptional signatures of peripheral blood response in patients with moderate COVID-19.|*Disease Progression[MESH]|*RNA-Seq[MESH]|Adult[MESH]|Aged[MESH]|COVID-19/*blood[MESH]|Cytokines/*blood[MESH]|Female[MESH]|Gene Expression Regulation[MESH]|Humans[MESH]|Inflammation Mediators/*blood[MESH]|Leukocytes, Mononuclear/*metabolism/virology[MESH]|Longitudinal Studies[MESH]|Male[MESH]|Middle Aged[MESH]
  
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