期刊
LIFE SCIENCE ALLIANCE
卷 4, 期 11, 页码 -出版社
LIFE SCIENCE ALLIANCE LLC
DOI: 10.26508/lsa.202101075
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资金
- Medical Research Council (MRC) [MR/M003493/1, MR/R001413/1]
- Cancer Research UK-University College London (CRUK-UCL) Centre [C416/A25145]
- National Institute for Health (NIHR) Biomedical Research Centres at Guy's & St Thomas' NHS Foundation Trust and King's College London
- MRC [MR/R001413/1] Funding Source: UKRI
The majority of T-bet target genes are conserved between mouse and human, either via preservation of binding sites or via alternative binding sites associated with transposon-linked insertion. Species-specific T-bet binding is associated with differences in transcription factor-binding motifs and species-specific expression of associated genes.
Gene expression programs controlled by lineage-determining transcription factors are often conserved between species. However, infectious diseases have exerted profound evolutionary pressure, and therefore the genes regulated by immune-specific transcription factors might be expected to exhibit greater divergence. T-bet (Tbx21) is the immune-specific, lineage-specifying transcription factor for T helper type I (Th1) immunity, which is fundamental for the immune response to intracellular pathogens but also underlies inflammatory diseases. We compared T-bet genomic targets between mouse and human CD4+ T cells and correlated T-bet binding patterns with species-specific gene expression. Remarkably, we found that the majority of T-bet target genes are conserved between mouse and human, either via preservation of binding sites or via alternative binding sites associated with transposon-linked insertion. Species-specific T-bet binding was associated with differences in transcription factor-binding motifs and species-specific expression of associated genes. These result s provide a genome-wi de cross-species comparison of Th1 gene regulation that will enable more accurate translation of genetic targets and therapeutics from pre-clinical models of inflammatory and infectious diseases and cancer into human clinical trials.
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