Type I IFN-dependent antibody response at the basis of sex dimorphism in the outcome of COVID-19.
Antibody response
COVID-19
Plasmacytoid dendritic cells
Sex-dimorphism
Type I IFN
Journal
Cytokine & growth factor reviews
ISSN: 1879-0305
Titre abrégé: Cytokine Growth Factor Rev
Pays: England
ID NLM: 9612306
Informations de publication
Date de publication:
04 2021
04 2021
Historique:
received:
24
09
2020
revised:
01
10
2020
accepted:
02
10
2020
pubmed:
20
10
2020
medline:
21
4
2021
entrez:
19
10
2020
Statut:
ppublish
Résumé
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the ongoing coronavirus disease 2019 (COVID-19) pandemic, induces severe pneumonia mainly in elderly males. Epidemiological data clearly indicate sex-based differences in disease outcomes, with men accounting for about 70 % of deaths, despite similar susceptibility to infection. It is well known that females are endowed with higher capacity to produce antibodies, which correlates with viral clearance and disease resolution in the context of SARS-Cov-2 infection. Many X-linked immune genes escape X inactivation showing biallelic expression in female immune cells, particularly in plasmacytoid dendritic cells (pDCs). PDCs are more active in females and endowed with high capability to induce IFN-α-mediated B cell activation and differentiation into antibody-producing plasma cells throughout epigenetic mechanisms linked to trained immunity. Thus, we hypothesize that following SARS-CoV-2 infection, epigenetic modifications of X-linked genes involved in pDC-mediated type I IFN (IFN-I) signaling occurs more effectively in females, for inducing neutralizing antibody response as an immune correlate driving sex-biased disease outcome.
Identifiants
pubmed: 33071044
pii: S1359-6101(20)30215-X
doi: 10.1016/j.cytogfr.2020.10.001
pmc: PMC7543933
pii:
doi:
Substances chimiques
Interferon Type I
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
66-74Informations de copyright
Copyright © 2020 Elsevier Ltd. All rights reserved.
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