{"entity": "researcher", "timestamp": "2026-09-30T03:46:29.660Z", "family": "Norin", "given": "Ulrika", "initials": "U", "orcid": "0000-0003-1063-6339", "affiliations": ["Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden. Ulrika_norin@hotmail.com."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/7d79bc148fd34a9894d6bb8e8d384530.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/7d79bc148fd34a9894d6bb8e8d384530"}}, "publications": [{"entity": "publication", "iuid": "bf91743a66e044b1adaee51b4574c80c", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/bf91743a66e044b1adaee51b4574c80c.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/bf91743a66e044b1adaee51b4574c80c"}}, "title": "Endophilin A2 deficiency protects rodents from autoimmune arthritis by modulating T cell activation.", "authors": [{"family": "Norin", "given": "Ulrika", "initials": "U", "orcid": "0000-0003-1063-6339", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/7d79bc148fd34a9894d6bb8e8d384530.json"}}, {"family": "Rintisch", "given": "Carola", "initials": "C"}, {"family": "Meng", "given": "Liesu", "initials": "L", "orcid": "0000-0003-1985-050X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/50d145587afd4171a6c27cd00abc2cd3.json"}}, {"family": "Forster", "given": "Florian", "initials": "F"}, {"family": "Ekman", "given": "Diana", "initials": "D"}, {"family": "Tuncel", "given": "Jonatan", "initials": "J"}, {"family": "Klocke", "given": "Katrin", "initials": "K"}, {"family": "B\u00e4cklund", "given": "Johan", "initials": "J"}, {"family": "Yang", "given": "Min", "initials": "M"}, {"family": "Bonner", "given": "Michael Y", "initials": "MY"}, {"family": "Lahore", "given": "Gonzalo Fernandez", "initials": "GF"}, {"family": "James", "given": "Jaime", "initials": "J"}, {"family": "Shchetynsky", "given": "Klementy", "initials": "K"}, {"family": "Bergquist", "given": "Maria", "initials": "M"}, {"family": "Gjertsson", "given": "Inger", "initials": "I"}, {"family": "Hubner", "given": "Norbert", "initials": "N", "orcid": "0000-0002-1218-6223", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5f8fcb2e3ce2473b8a89b74727da5bb0.json"}}, {"family": "B\u00e4ckdahl", "given": "Liselotte", "initials": "L"}, {"family": "Holmdahl", "given": "Rikard", "initials": "R", "orcid": "0000-0002-4969-2576", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/aef6264212044f46a28c24d5fc147438.json"}}], "type": "journal article", "published": "2021-01-27", "journal": {"title": "Nat Commun", "issn": "2041-1723", "volume": "12", "issue": "1", "pages": "610", "issn-l": "2041-1723"}, "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.", "doi": "10.1038/s41467-020-20586-2", "pmid": "33504785", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC7840939"}, {"db": "pii", "key": "10.1038/s41467-020-20586-2"}], "notes": [], "created": "2026-09-23T12:02:44.385Z", "modified": "2026-09-23T12:02:44.495Z"}]}