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Title

Deregulated cellular circuits driving immunoglobulins and complement consumption associate with the severity of COVID‐19 patients

AuthorsMarcos Jiménez, Ana; Sánchez‐Alonso, Santiago; Alcaraz‐Serna, Ana; Esparcia, Laura; López‐Sanz, Celia; Sampedro-Nuñez, Miguel; Mateu‐Albero, Tamara; Sánchez‐Cerrillo, Ildefonso; Martínez‐Fleta, Petra; Gabrie, Ligia; Campo Guerola, Luciana del; Rodríguez Frade, José M.; Casasnovas, José María ; Reyburn, H. T. ; Valés-Gómez, Mar; López Trascasa, Margarita; Martín‐Gayo, Enrique; Calzada, María José; Castañeda, Santos; Fuente, Hortensia de la; González‐Álvaro, Isidoro; Sánchez‐Madrid, Francisco; Muñoz‐Calleja, Cecilia; Alfranca, Arántzazu
KeywordsCOVID-19
SARS-CoV-2
Immunity
Complement
Immunoglobulins
Issue Date30-Nov-2020
PublisherJohn Wiley & Sons
CitationEuropean Journal of Immunology (2020)
AbstractSARS‐CoV‐2 infection causes an abrupt response by the host immune system, which is largely responsible for the outcome of COVID‐19. We investigated whether the specific immune responses in the peripheral blood of 276 patients associated to severity and progression of COVID‐19. At admission, dramatic lymphopenia of T, B and NK cells associated to severity. Conversely, the proportion of B cells, plasmablasts, circulating follicular helper T cells (cTfh) and CD56‐CD16+ NK‐cells increased. Regarding humoral immunity, levels of IgM, IgA and IgG were unaffected, but when degrees of severity were considered, IgG was lower in severe patients. Compared to healthy donors, complement C3 and C4 protein levels were higher in mild and moderate, but not in severe patients, while the activation peptide of C5 (C5a) increased from the admission in every patient, regardless their severity. Moreover, total IgG, the IgG1 and IgG3 isotypes and C4 decreased from day 0 to day 10 in patients who were hospitalized for more than two weeks, but not in patients who were discharged earlier. Our study provides important clues to understand the immune response observed in COVID‐19 patients, associating severity with an imbalanced humoral response and identifying new targets for therapeutic intervention.
Publisher version (URL)https://doi.org/10.1002/eji.202048858
URIhttp://hdl.handle.net/10261/224845
DOI10.1002/eji.202048858
ISSN0014-2980
E-ISSN1521-4141
Appears in Collections:(CNB) Artículos
(VICYT) Colección Especial COVID-19
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