ArticleNature communications2025
An essential role for TASL in mouse autoimmune pathogenesis and Toll-like receptor signaling.
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 11 papers.
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Who cites it
11 citing papers in PubMed.
- Jianpi Zishen Decoction ameliorates renal damage induced by systemic lupus erythematosus through inhibition of the TLR4/MAPK pathway.Pharmaceutical biology · 2026Article
- The SLC15A4-TASL complex is essential for lupus development in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- TLR7 in systemic lupus erythematosus: genetics and emerging therapies.Nature reviews. Rheumatology · 2026Review
- The Pharmacology of the SLC15A4-TASL Complex, an Emerging Target for the Treatment of Lupus.Pharmacology research & perspectives · 2026Review
- Female mice with a Xist deletion in B cells can develop lupus-associated phenotypes.Cell reports · 2026Article
- The adaptor protein TASL is required for age-related B cell emergence and lupus-like disease development in mice.PLoS biology · 2026Article
- Long noncoding RNA regulation of immunity.Nature immunology · 2026Review
- The type 1 and type 3 immune responses underlying the tissue inflammation associated with NOX2 deficiency.Frontiers in immunology · 2026Review
- Truncated APC impairs innate immune response by targeting MAVS on mitochondria in colorectal cancer.Journal of translational medicine · 2025Article
- S-TIR-ring up TLR7 and TLR9: signaling domain substitutions clarify the TLR paradox.The Journal of clinical investigation · 2025Article
- More X's, more problems: how contributions from the X chromosomes enhance female predisposition for autoimmunity.Current opinion in immunology · 2025Review
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TASL is an immune adaptor that binds to the solute carrier SLC15A4 and facilitates activation of the transcription factor IRF5 during Toll-like receptor (TLR) signaling. Similar to IRF5 and SLC15A4, single nucleotide polymorphisms (SNPs) within TASL have been implicated in increased susceptibility to systemic lupus erythematosus (SLE) in patients. However, the biological function of TASL in vivo and how SLE-associated SNPs increase disease risk is unknown. Here we report that mice deficient in Tasl lack responses to TLR7/9 stimulation and are protected from autoimmune symptoms induced by Aldara or pristane. Loss of Tasl reduces IRF5 phosphorylation and cytokine production in multiple immune cell types but has no effect on other aspects of TLR signaling. Conversely, an SLE-associated TASL risk variant increases TASL protein expression via codon usage, resulting in augmented cytokine production in human cells. Altogether, our study validates the essential function of TASL in TLR signaling and autoimmune pathogenesis.
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