Neonatal genetics of gene expression reveal potential origins of autoimmune and allergic disease risk

Qin Qin Huang (), Howard H. F. Tang, Shu Mei Teo, Danny Mok, Scott C. Ritchie, Artika P. Nath, Marta Brozynska, Agus Salim, Andrew Bakshi, Barbara J. Holt, Chiea Chuen Khor, Peter D. Sly, Patrick G. Holt, Kathryn E. Holt and Michael Inouye ()
Additional contact information
Qin Qin Huang: Baker Heart and Diabetes Institute
Howard H. F. Tang: Baker Heart and Diabetes Institute
Shu Mei Teo: Baker Heart and Diabetes Institute
Danny Mok: The University of Western Australia
Scott C. Ritchie: Baker Heart and Diabetes Institute
Artika P. Nath: Baker Heart and Diabetes Institute
Marta Brozynska: Baker Heart and Diabetes Institute
Agus Salim: Baker Heart and Diabetes Institute
Andrew Bakshi: Monash University
Barbara J. Holt: The University of Western Australia
Chiea Chuen Khor: Genome Institute of Singapore, Agency for Science, Technology and Research
Peter D. Sly: The University of Queensland
Patrick G. Holt: The University of Western Australia
Kathryn E. Holt: Monash University
Michael Inouye: Baker Heart and Diabetes Institute

Nature Communications, 2020, vol. 11, issue 1, 1-12

Abstract: Abstract Chronic immune-mediated diseases of adulthood often originate in early childhood. To investigate genetic associations between neonatal immunity and disease, we map expression quantitative trait loci (eQTLs) in resting myeloid cells and CD4+ T cells from cord blood samples, as well as in response to lipopolysaccharide (LPS) or phytohemagglutinin (PHA) stimulation, respectively. Cis-eQTLs are largely specific to cell type or stimulation, and 31% and 52% of genes with cis-eQTLs have response eQTLs (reQTLs) in myeloid cells and T cells, respectively. We identified cis regulatory factors acting as mediators of trans effects. There is extensive colocalisation between condition-specific neonatal cis-eQTLs and variants associated with immune-mediated diseases, in particular CTSH had widespread colocalisation across diseases. Mendelian randomisation shows causal neonatal gene expression effects on disease risk for BTN3A2, HLA-C and others. Our study elucidates the genetics of gene expression in neonatal immune cells, and aetiological origins of autoimmune and allergic diseases.

Date: 2020
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DOI: 10.1038/s41467-020-17477-x

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