학술논문
IgG immune complexes may contribute to neutrophil activation in the course of severe COVID-19.
Document Type
Journal Article
Author
Mazzitelli, Ignacio; Bleichmar, Lucia; Ludueña, María Guillermina; Pisarevsky, Andrea; Labato, Mariana; Chiaradia, Verónica; Finocchieto, Paola; Paulin, Francisco; Hormanstorfer, Macarena; Baretto, María Constanza; Adanza, Santiago Piombi; Parodi, María Noel; Ragusa, Martín; Melucci, Claudia; Díaz, Fernando Erra; Paletta, Ana; Diego, Facundo Di; Ceballos, Ana; Geffner, Jorge; Di Diego, Facundo
Source
Subject
*COVID-19
*IMMUNE complexes
*IMMUNOGLOBULIN G
*BLOOD lactate
*LACTATE dehydrogenase
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Language
ISSN
0022-1899
Abstract
Severe COVID-19 is associated with an overactive inflammatory response mediated by macrophages. Here, we analyzed the phenotype and function of neutrophils in COVID-19 patients. We found that neutrophils from severe COVID-19 patients express high levels of CD11b and CD66b, spontaneously produce CXCL8 and CCL2 and show a strong association with platelets. Production of CXCL8 correlated with plasmatic concentrations of LDH and D-dimer. Whole blood assays revealed that neutrophils from severe COVID-19 patients show a clear association with IgG immune complexes. Moreover, we found that sera from severe patients contain high levels of immune complexes and activate neutrophils through a mechanism partially dependent on FcγRII (CD32). Interestingly, when integrated in immune complexes, anti-SARS-CoV-2 IgG antibodies from severe patients displayed a higher pro-inflammatory profile compared with antibodies from mild patients. Our study suggests that IgG immune complexes might promote the acquisition of an inflammatory signature by neutrophils worsening the course of COVID-19. [ABSTRACT FROM AUTHOR]