A study using single-cell transcriptomics and mapping of expression quantitative trait loci (eQTLs) in a dynamic model of CD4+ T cell activation reveals novel, context-specific eQTLs linked to genes associated with immune diseases such as inflammatory bowel disease.
This is a preview of subscription content, access via your institution
Access options
Access Nature and 54 other Nature Portfolio journals
Get Nature+, our best-value online-access subscription
$29.99 / 30 days
cancel any time
Subscribe to this journal
Receive 12 print issues and online access
$209.00 per year
only $17.42 per issue
Rent or buy this article
Prices vary by article type
from$1.95
to$39.95
Prices may be subject to local taxes which are calculated during checkout

References
Cano-Gamez, E. et al. Single-cell transcriptomics identifies an effectorness gradient shaping the response of CD4+ T cells to cytokines. Nat. Commun. 11, 1801 (2020). Though the use of single-cell transcriptomics, this work demonstrated that T cells form a continuum of cell types and states.
Soskic, B. et al. Chromatin activity at GWAS loci identifies T cell states driving complex immune diseases. Nat. Genet. 51, 1486–1493 (2019). This work showed that immune-disease variants undergo enrichment for active chromatin regions that are upregulated after T cell activation.
Fang, H. et al. A genetics-led approach defines the drug target landscape of 30 immune-related traits. Nat. Genet. 51, 1082–1091 (2019). This work used a genetics-led approach to identify known drug targets for immune traits and nominate new ones.
Additional information
Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
This is a summary of: Soskic, B. et al. Immune disease risk variants regulate gene expression dynamics during CD4+ T cell activation. Nat. Genet. https://doi.org/10.1038/s41588-022-01066-3 (2022).
Rights and permissions
About this article
Cite this article
A molecular map of T cell activation gives insights into immune disease. Nat Genet 54, 752–753 (2022). https://doi.org/10.1038/s41588-022-01067-2
Published:
Issue Date:
DOI: https://doi.org/10.1038/s41588-022-01067-2