ArticleNature communications2025
Transposon invasion of primate genomes shaped human inflammatory enhancers and susceptibility to inflammatory diseases.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Human Alu loci gain enhancer-type epigenetic modifications in monocytes during response to bacterial LPS.Epigenetics & chromatin · 2026Article
- Quantitative Control of Transposable Elements: From Genome Plasticity to Immune Regulatory Circuits.Cell biochemistry and function · 2026Review
- Review
- Multiomic Profiling Reveals the Regulation of Many Immune-Related Genes by PU.1 in Porcine Alveolar Macrophages.Animals : an open access journal from MDPI · 2026Article
- Transposable elements as a possible missing link between genetic predisposition and environmental triggers of autoimmune disorders: insights from type 1 diabetes, systemic lupus erythematosus and rheumatoid arthritis.Frontiers in immunology · 2026Review
- PervasivebioRxiv : the preprint server for biology · 2025Article
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Authors and funding
4 authors.
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Abstract
Human inflammatory response reflects adaptive alteration of immune-cell regulatory elements during human evolution. Yet the impact of the deeper evolutionary history of these elements, within primate genomes reshaped by transposon expansions, remains unclear. Tracing sequence changes in human immune-cell enhancers back to macaque and analysing proinflammatory transcription factor binding, we show that primate-specific endogenous retroviruses and Alu transposons introduced functional NF-κB and IRF1 motifs, contributing most to the great-ape-specific pool. After the human-macaque split, these motifs tend to evolve toward higher predicted binding affinity. In modern humans, positive selection favoured alleles, often Alu-derived, that increase enhancer affinity for NF-κB, and Alu-containing enhancers are enriched in signatures of adaptation. Highly mutable, Alus disproportionately contribute to the pool of adaptive alleles, including at enhancers linked to inflammatory diseases. We propose that primate-specific transposons facilitated the evolution of inflammatory responses in great apes, with Alus shaping adaptive potential in modern humans.
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