ArticleNature communications2024
Erythroid-intrinsic activation of TLR8 impairs erythropoiesis in inherited anemia.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- TLR8 gain-of-function syndrome.Journal of human immunity · 2026Article
- Artificial intelligence-driven magnetic property prediction and materials discovery for next-generation spintronics.RSC advances · 2026Review
- TLR7 in systemic lupus erythematosus: genetics and emerging therapies.Nature reviews. Rheumatology · 2026Review
- Glycosylated NS3/NS3A protein of bluetongue virus facilitates efficient viral egress via lipid raft anchoring.Journal of virology · 2026Article
- Clinical characteristics, management, and hematopoietic cell transplantation of patients with TLR8 gain-of-function.Blood advances · 2026Article
- Structural modeling and functional characterization of a novel gain-of-function TLR8 variant causing severe inflammatory syndrome.JCI insight · 2026Article
- Review
- Ancient genomic linkage of α-globin and Nprl3 couples metabolism with erythropoiesis.Nature communications · 2025Article
- Discovery of Novel Isoxazole-Based Small-Molecule Toll-Like Receptor 8 Antagonists.Journal of medicinal chemistry · 2025Article
- Article
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Authors and funding
26 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inherited non-hemolytic anemia is a group of rare bone marrow disorders characterized by erythroid defects. Although concerted efforts have been made to explore the underlying pathogenetic mechanisms of these diseases, the understanding of the causative mutations are still incomplete. Here we identify in a diseased pedigree that a gain-of-function mutation in toll-like receptor 8 (TLR8) is implicated in inherited non-hemolytic anemia. TLR8 is expressed in erythroid lineage and erythropoiesis is impaired by TLR8 activation whereas enhanced by TLR8 inhibition from erythroid progenitor stage. Mechanistically, TLR8 activation blocks annexin A2 (ANXA2)-mediated plasma membrane localization of STAT5 and disrupts EPO signaling in HuDEP2 cells. TLR8 inhibition improves erythropoiesis in RPS19
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