The genetic basis of autoimmunity seen through the lens of T cell functional traits

Kaitlyn A. Lagattuta, Hannah L. Park, Laurie Rumker, Kazuyoshi Ishigaki, Aparna Nathan () and Soumya Raychaudhuri ()
Additional contact information
Kaitlyn A. Lagattuta: Harvard Medical School
Hannah L. Park: Harvard Medical School
Laurie Rumker: Harvard Medical School
Kazuyoshi Ishigaki: Harvard Medical School
Aparna Nathan: Harvard Medical School
Soumya Raychaudhuri: Harvard Medical School

Nature Communications, 2024, vol. 15, issue 1, 1-6

Abstract: Abstract Autoimmune disease heritability is enriched in T cell-specific regulatory regions of the genome. Modern-day T cell datasets now enable association studies between single nucleotide polymorphisms (SNPs) and a myriad of molecular phenotypes, including chromatin accessibility, gene expression, transcriptional programs, T cell antigen receptor (TCR) amino acid usage, and cell state abundances. Such studies have identified hundreds of quantitative trait loci (QTLs) in T cells that colocalize with genetic risk for autoimmune disease. The key challenge facing immunologists today lies in synthesizing these results toward a unified understanding of the autoimmune T cell: which genes, cell states, and antigens drive tissue destruction?

Date: 2024
References: View references in EconPapers View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-024-45170-w Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-45170-w

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-024-45170-w

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().