% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Zhang:303377,
      author       = {Z. Zhang and W. Li and Q. Zhan and M. Aillaud and J.
                      Botey-Bataller and M. Zoodsma and R. Ter Horst and L. A. B.
                      Joosten and C. Bock and L. N. Schulte and C.-J. Xu and M. G.
                      Netea and M. J. Bonder$^*$ and Y. Li},
      title        = {{U}nveiling genetic signatures of immune response in
                      immune-related diseases through single-cell e{QTL} analysis
                      across diverse conditions.},
      journal      = {Nature Communications},
      volume       = {16},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-01626},
      pages        = {7134},
      year         = {2025},
      abstract     = {Deciphering the intricate regulatory mechanisms underlying
                      biological processes holds promise for elucidating how
                      genetic variants contribute to immune-related disorders. We
                      map genetic effects on gene expression (expression
                      quantitative trait locus, eQTL) using single-cell
                      transcriptomes of 152 samples from 38 healthy individuals,
                      covering baseline state and lipopolysaccharide challenge
                      either before or after Bacillus Calmette-Guerin vaccination.
                      Interestingly, we uncover a monocyte eQTL linked to the
                      LCP1, shedding light on inter-individual variations in
                      trained immunity. Furthermore, we elucidate genetic and
                      epigenetic regulatory networks of CD55 and SLFN5. Of note,
                      our results support the pivotal roles of SLFN5 in COVID-19
                      pathogenesis by incorporating disease-associated loci,
                      chromatin accessibility, and transcription factor binding
                      affinities, aligning with the established functions of SLFN5
                      in restricting virus replication during viral infection. Our
                      study provides a paradigm to decipher genetic underpinnings
                      of complex traits by integrating single-cell eQTLs with
                      multi-omics data from patients and public databases.},
      keywords     = {Humans / Quantitative Trait Loci: genetics / Single-Cell
                      Analysis: methods / COVID-19: immunology / COVID-19:
                      genetics / COVID-19: virology / SARS-CoV-2: immunology /
                      Transcriptome / Male / Female / Gene Regulatory Networks /
                      Monocytes: immunology / Monocytes: metabolism / Immune
                      System Diseases: genetics / Immune System Diseases:
                      immunology / Adult / Immunity: genetics / Genetic
                      Predisposition to Disease},
      cin          = {B260},
      ddc          = {500},
      cid          = {I:(DE-He78)B260-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40759647},
      doi          = {10.1038/s41467-025-61192-4},
      url          = {https://inrepo02.dkfz.de/record/303377},
}