B cell phenotype and serum levels of interferons, BAFF, and APRIL in multisystem inflammatory syndrome in children associated with COVID-19 (MIS-C)

0577594 - ÚOCHB 2024 RIV DE eng J - Journal Article
Klocperk, A. - Bloomfield, M. - Paráčková, Z. - Aillot, Ludovic - Fremuth, J. - Šašek, L. - David, J. - Fencl, F. - Skotnicová, A. - Rejlová, K. - Magner, M. - Hrušák, O. - Šedivá, A.
B cell phenotype and serum levels of interferons, BAFF, and APRIL in multisystem inflammatory syndrome in children associated with COVID-19 (MIS-C).
Molecular and Cellular Pediatrics. Roč. 10, č. 1 (2023), č. článku 15. ISSN 2194-7791
Institutional support: RVO:61388963
Keywords : PIMS-TS * MIS-C * COVID-19 * interferon * BAFF * APRIL * SLE
OECD category: Virology
Method of publishing: Open access
https://doi.org/10.1186/s40348-023-00169-z

Background: Multisystem inflammatory syndrome in children associated with COVID-19 (MIS-C) is a late complication of pediatric COVID-19, which follows weeks after the original SARS-CoV-2 infection, regardless of its severity. It is characterized by hyperinflammation, neutrophilia, lymphopenia, and activation of T cells with elevated IFN-γ. Observing the production of autoantibodies and parallels with systemic autoimmune disorders, such as systemic lupus erythematodes (SLE), we explored B cell phenotype and serum levels of type I, II, and III interferons, as well as the cytokines BAFF and APRIL in a cohort of MIS-C patients and healthy children after COVID-19. Results: We documented a significant elevation of IFN-γ, but not IFN-α and IFN-λ in MIS-C patients. BAFF was elevated in MIS-C patient sera and accompanied by decreased BAFFR expression on all B cell subtypes. The proportion of plasmablasts was significantly lower in patients compared to healthy post-COVID children. We noted the pre-IVIG presence of ENA Ro60 autoantibodies in 4/35 tested MIS-C patients. Conclusions: Our work shows the involvement of humoral immunity in MIS-C and hints at parallels with the pathophysiology of SLE, with autoreactive B cells driven towards autoantibody production by elevated BAFF.
Permanent Link: https://hdl.handle.net/11104/0346730