ArticleNature communications2021
Endophilin A2 deficiency protects rodents from autoimmune arthritis by modulating T cell activation.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- TLR9-engineered photoresponsive biomimetic nanodecoys for targeted NETs clearance to mitigate periodontitis-associated bone resorption.International journal of oral science · 2026Article
- Targeting SH3GL1 for prognosis and immune response in breast cancer.Journal of pharmaceutical analysis · 2026Article
- Bending the boundaries: the many facets of endophilin-As from membrane dynamics to disease.Cellular and molecular life sciences : CMLS · 2025Review
- Whole-genome sequencing reveals the impact of lipid pathway and APOE genotype on brain amyloidosis.Human molecular genetics · 2025Article
- SH3GL1-activated FTH1 inhibits ferroptosis and confers doxorubicin resistance in diffuse large B-cell lymphoma.Clinical and translational medicine · 2025Article
- Endophilin A2 Deficiency Impairs Antibody Production in Humans.Journal of clinical immunology · 2024Article
- Biology of endophilin and it's role in disease.Frontiers in immunology · 2023Review
- The interplay between membrane topology and mechanical forces in regulating T cell receptor activity.Communications biology · 2022Review
- Recent Advances in Understanding the Pathogenesis of Rheumatoid Arthritis: New Treatment Strategies.Cells · 2021Review
Corrections and comments
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Authors and funding
18 authors at 7 institutions in 3 countries.
Funding
Abstract
The introduction of the CTLA-4 recombinant fusion protein has demonstrated therapeutic effects by selectively modulating T-cell activation in rheumatoid arthritis. Here we show, using a forward genetic approach, that a mutation in the SH3gl1 gene encoding the endocytic protein Endophilin A2 is associated with the development of arthritis in rodents. Defective expression of SH3gl1 affects T cell effector functions and alters the activation threshold of autoreactive T cells, thereby leading to complete protection from chronic autoimmune inflammatory disease in both mice and rats. We further show that SH3GL1 regulates human T cell signaling and T cell receptor internalization, and its expression is upregulated in rheumatoid arthritis patients. Collectively our data identify SH3GL1 as a key regulator of T cell activation, and as a potential target for treatment of autoimmune diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.