{"entity": "researcher", "timestamp": "2026-09-30T23:44:08.310Z", "family": "Yang", "given": "Min", "initials": "M", "orcid": "0000-0002-3224-5999", "affiliations": ["Section for Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/89e1ae8c58224a99805287fd2a01db01.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/89e1ae8c58224a99805287fd2a01db01"}}, "publications": [{"entity": "publication", "iuid": "d1f7c79dae48430a89d0c40a86e825d5", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/d1f7c79dae48430a89d0c40a86e825d5.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/d1f7c79dae48430a89d0c40a86e825d5"}}, "title": "Regulatory T cells control epitope spreading in autoimmune arthritis independent of cytotoxic T-lymphocyte antigen-4.", "authors": [{"family": "Yang", "given": "Min", "initials": "M", "orcid": "0000-0002-3224-5999", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/89e1ae8c58224a99805287fd2a01db01.json"}}, {"family": "Klocke", "given": "Katrin", "initials": "K"}, {"family": "Hernandez", "given": "Clara Marquina", "initials": "CM"}, {"family": "Xu", "given": "Bingze", "initials": "B"}, {"family": "Gjertsson", "given": "Inger", "initials": "I"}, {"family": "Wing", "given": "Kajsa", "initials": "K"}, {"family": "Holmdahl", "given": "Rikard", "initials": "R"}], "type": "journal article", "published": "2018-12-00", "journal": {"title": "Immunology", "issn": "1365-2567", "volume": "155", "issue": "4", "pages": "446-457", "issn-l": "0019-2805"}, "abstract": "CD4+ Foxp3+ regulatory T (Treg) cells can control both cellular and humoral immune responses; however, when and how Treg cells play a predominant role in regulating autoimmune disease remains elusive. To deplete Treg cells in vivo at given time-points, we used a mouse strain, susceptible to glucose-6-phosphate isomerase peptide-induced arthritis (GIA), in which the deletion of Treg cells can be controlled by diphtheria toxin treatment. By depleting Treg cells in the GIA mouse model, we found that a temporary lack of Treg cells at both priming and onset exaggerated disease development. Ablation of Treg cells led to the expansion of antigen-specific CD4+ T cells including granulocyte-macrophage colony-stimulating factor, interferon-\u03b3 and interleukin-17-producing T cells, and promoted both T-cell and B-cell epitope spreading, which perpetuated arthritis. Interestingly, specific depletion of cytotoxic T-lymphocyte antigen-4 (CTLA-4) on Treg cells only, was sufficient to protect mice from GIA, due to the expansion of CTLA-4- Treg cells expressing alternative suppressive molecules. Collectively, our findings suggest that Treg cells, independently of CTLA-4, act as the key driving force in controlling autoimmune arthritis development.", "doi": "10.1111/imm.12983", "pmid": "29992549", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC6231009"}], "notes": [], "created": "2026-09-23T12:51:09.940Z", "modified": "2026-09-23T12:51:10.040Z"}]}