ArticlePloS one2021
The peptide symporter SLC15a4 is essential for the development of systemic lupus erythematosus in murine models.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- 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
- The Pharmacology of the SLC15A4-TASL Complex, an Emerging Target for the Treatment of Lupus.Pharmacology research & perspectives · 2026Review
- TLR7 in systemic lupus erythematosus: genetics and emerging therapies.Nature reviews. Rheumatology · 2026Review
- Lysosomal checkpoints in renal autoimmunity: from antigen processing to metabolic-immune crosstalk.Frontiers in immunology · 2026Review
- The Role of Solute Carriers in the Metabolic Reprogramming of Skin Diseases.Clinical reviews in allergy & immunology · 2025Review
- Development of conformation-selective antibodies targeting human SLC15A4.Nature communications · 2025Article
- Immunometabolism in systemic lupus erythematosus.Nature reviews. Rheumatology · 2025Review
- Nucleic acid triggers of autoimmunity and autoinflammation.Current opinion in immunology · 2025Review
- The TLR7/9 adaptors TASL and TASL2 mediate IRF5-dependent antiviral responses and autoimmunity in mouse.Nature communications · 2025Article
- Chemoproteomic development of SLC15A4 inhibitors with anti-inflammatory activity.Nature chemical biology · 2024Article
- Transient Co-expression of Membrane Protein Complexes in Mammalian Cells.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Structural basis for recruitment of TASL by SLC15A4 in human endolysosomal TLR signaling.Nature communications · 2023Article
- A conformation-locking inhibitor of SLC15A4 with TASL proteostatic anti-inflammatory activity.Nature communications · 2023Article
- Molecular basis of TASL recruitment by the peptide/histidine transporter 1, PHT1.Nature communications · 2023Article
- Metabolic control from the endolysosome: lysosome-resident amino acid transporters open novel therapeutic possibilities.Frontiers in immunology · 2023Review
- A Non-Coding Variant inFrontiers in lupus · 2023Article
- Identification ofInternational journal of molecular sciences · 2022Article
- The solute carrier SLC15A4 is required for optimal trafficking of nucleic acid-sensing TLRs and ligands to endolysosomes.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- miR-31-5p Regulates Type I Interferon by Targeting SLC15A4 in Plasmacytoid Dendritic Cells of Systemic Lupus Erythematosus.Journal of inflammation research · 2022Article
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Authors and funding
18 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease representing a serious unmet medical need. The disease is associated with the loss of self-tolerance and exaggerated B cell activation, resulting in autoantibody production and the formation of immune complexes that accumulate in the kidney, causing glomerulonephritis. TLR7, an important mediator of the innate immune response, drives the expression of type-1 interferon (IFN), which leads to expression of type-1 IFN induced genes and aggravates lupus pathology. Because the lysosomal peptide symporter slc15a4 is critically required for type-1 interferon production by pDC, and for certain B cell functions in response to TLR7 and TLR9 signals, we considered it as a potential target for pharmacological intervention in SLE. We deleted the slc15a4 gene in C57BL/6, NZB, and NZW mice and found that pristane-challenged slc15a4-/- mice in the C57BL/6 background and lupus prone slc15a4-/- NZB/W F1 mice were both completely protected from lupus like disease. In the NZB/W F1 model, protection persisted even when disease development was accelerated with an adenovirus encoding IFNα, emphasizing a broad role of slc15a4 in disease initiation. Our results establish a non-redundant function of slc15a4 in regulating both innate and adaptive components of the immune response in SLE pathobiology and suggest that it may be an attractive drug target.
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