COVID-19 genetic risk variants are associated with expression of multiple genes in diverse immune cell types
Benjamin J. Schmiedel,
Job Rocha,
Cristian Gonzalez-Colin,
Sourya Bhattacharyya,
Ariel Madrigal,
Christian H. Ottensmeier,
Ferhat Ay,
Vivek Chandra and
Pandurangan Vijayanand ()
Additional contact information
Benjamin J. Schmiedel: La Jolla Institute for Immunology
Job Rocha: La Jolla Institute for Immunology
Cristian Gonzalez-Colin: La Jolla Institute for Immunology
Sourya Bhattacharyya: La Jolla Institute for Immunology
Ariel Madrigal: La Jolla Institute for Immunology
Christian H. Ottensmeier: La Jolla Institute for Immunology
Ferhat Ay: La Jolla Institute for Immunology
Vivek Chandra: La Jolla Institute for Immunology
Pandurangan Vijayanand: La Jolla Institute for Immunology
Nature Communications, 2021, vol. 12, issue 1, 1-12
Abstract:
Abstract Common genetic polymorphisms associated with COVID-19 illness can be utilized for discovering molecular pathways and cell types driving disease pathogenesis. Given the importance of immune cells in the pathogenesis of COVID-19 illness, here we assessed the effects of COVID-19-risk variants on gene expression in a wide range of immune cell types. Transcriptome-wide association study and colocalization analysis revealed putative causal genes and the specific immune cell types where gene expression is most influenced by COVID-19-risk variants. Notable examples include OAS1 in non-classical monocytes, DTX1 in B cells, IL10RB in NK cells, CXCR6 in follicular helper T cells, CCR9 in regulatory T cells and ARL17A in TH2 cells. By analysis of transposase accessible chromatin and H3K27ac-based chromatin-interaction maps of immune cell types, we prioritized potentially functional COVID-19-risk variants. Our study highlights the potential of COVID-19 genetic risk variants to impact the function of diverse immune cell types and influence severe disease manifestations.
Date: 2021
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-26888-3
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DOI: 10.1038/s41467-021-26888-3
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