{"entity": "researcher", "timestamp": "2026-08-14T12:30:09.969Z", "family": "Gister\u00e5", "given": "Anton", "initials": "A", "orcid": "0000-0002-4614-8030", "affiliations": ["Department of Medicine, Center for Molecular Medicine, Solna, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden."], "links": {"self": {"href": "https://publications.scilifelab.se/researcher/3e2beec3559745a6ba1859252df4a547.json"}, "display": {"href": "https://publications.scilifelab.se/researcher/3e2beec3559745a6ba1859252df4a547"}}, "publications": [{"entity": "publication", "iuid": "ee2e0ed6e5fc4e969acfc7bd207dfefe", "links": {"self": {"href": "https://publications.scilifelab.se/publication/ee2e0ed6e5fc4e969acfc7bd207dfefe.json"}, "display": {"href": "https://publications.scilifelab.se/publication/ee2e0ed6e5fc4e969acfc7bd207dfefe"}}, "title": "Progenitor exhausted PD-1+ T cells are cellular targets of immune checkpoint inhibition in atherosclerosis.", "authors": [{"family": "Mulholland", "given": "Megan", "initials": "M", "orcid": "0000-0002-3352-0403", "researcher": {"href": "https://publications.scilifelab.se/researcher/332a484487504958849ef563550cd8a0.json"}}, {"family": "Chalou", "given": "Anthi", "initials": "A", "orcid": "0009-0008-4969-3262", "researcher": {"href": "https://publications.scilifelab.se/researcher/5294de2282b44506977b10f1f8da6f47.json"}}, {"family": "Andersson", "given": "Samuel H A", "initials": "SHA", "orcid": "0009-0009-7497-9403", "researcher": {"href": "https://publications.scilifelab.se/researcher/863588877fc848ca96ba6b2e66c9086a.json"}}, {"family": "Depuydt", "given": "Marie A C", "initials": "MAC", "orcid": "0000-0002-7174-1952", "researcher": {"href": "https://publications.scilifelab.se/researcher/1725c990029e403fb7b0c228b112f418.json"}}, {"family": "Yu", "given": "Yinda", "initials": "Y"}, {"family": "Lin", "given": "Shiying", "initials": "S"}, {"family": "Tallb\u00e4ck", "given": "Klara", "initials": "K", "orcid": "0009-0009-4506-6330", "researcher": {"href": "https://publications.scilifelab.se/researcher/1210f8d35a2d480d839300492143a8bc.json"}}, {"family": "Ericsson", "given": "Astrid", "initials": "A"}, {"family": "Jakobsson", "given": "Gabriel", "initials": "G", "orcid": "0000-0001-5071-9505", "researcher": {"href": "https://publications.scilifelab.se/researcher/99f0995b89884f6eb8d33e0e51c33800.json"}}, {"family": "de Mol", "given": "Jill", "initials": "J", "orcid": "0000-0003-3541-9912", "researcher": {"href": "https://publications.scilifelab.se/researcher/7c34c673397547b4bcecf3994d44882a.json"}}, {"family": "Kryvokhyzha", "given": "Dmytro", "initials": "D"}, {"family": "Lichtman", "given": "Andrew H", "initials": "AH", "orcid": "0000-0002-3546-058X", "researcher": {"href": "https://publications.scilifelab.se/researcher/c22011616511413b8c9f22be31a1f951.json"}}, {"family": "Foks", "given": "Amanda C", "initials": "AC", "orcid": "0000-0002-9747-3458", "researcher": {"href": "https://publications.scilifelab.se/researcher/d6713b7fbb8942bea6789bc4e07d575c.json"}}, {"family": "Schiopu", "given": "Alexandru", "initials": "A", "orcid": "0000-0002-7587-5050", "researcher": {"href": "https://publications.scilifelab.se/researcher/c7d2edf9030a445583f692dc4d884b7f.json"}}, {"family": "Bj\u00f6rkbacka", "given": "Harry", "initials": "H", "orcid": "0000-0003-3918-0857", "researcher": {"href": "https://publications.scilifelab.se/researcher/9f4c07bc840f491d843f67a9932d5f3a.json"}}, {"family": "Sl\u00fctter", "given": "Bram", "initials": "B", "orcid": "0000-0003-3996-0503", "researcher": {"href": "https://publications.scilifelab.se/researcher/aa4acafdcb714986a064c0c0369bd4f8.json"}}, {"family": "Gister\u00e5", "given": "Anton", "initials": "A", "orcid": "0000-0002-4614-8030", "researcher": {"href": "https://publications.scilifelab.se/researcher/3e2beec3559745a6ba1859252df4a547.json"}}, {"family": "Engelbertsen", "given": "Daniel", "initials": "D", "orcid": "0000-0002-0289-5210", "researcher": {"href": "https://publications.scilifelab.se/researcher/fc4f0e42f9444337adb276360c27c5cc.json"}}], "type": "journal article", "published": "2025-10-00", "journal": {"title": "Nat Cardiovasc Res", "issn": "2731-0590", "volume": "4", "issue": "10", "pages": "1311-1328", "issn-l": null}, "abstract": "Immune checkpoint inhibitors (ICIs), targeting checkpoint receptors such as programmed cell death protein 1 (PD-1), are associated with increased risk of cardiovascular events, but the underlying mechanisms remain poorly understood. Here we show that PD-1+ T cells from murine atherosclerotic aortas mainly display a progenitor exhausted phenotype (PD-1intSlamf6+Tim3-), produce IFN\u03b3 in vivo, exhibit signs of recent proliferation and maintain polyfunctionality. PD-1 blockade induced marked changes in plaque immune phenotype, with increased PD-1high T cell accumulation, IFN\u03b3 production, formation of lymphocyte foci and neutrophil recruitment. Depletion of PD-1high T cells prior to PD-1 blockade did not impede T cell recruitment, suggesting a role for progenitor exhausted PD-1int T cells in ICI-driven T cell plaque accumulation. Human circulating PD-1+ T cells produced IFN\u03b3 and were associated with subclinical coronary atherosclerosis. Our studies highlight IFN\u03b3-producing PD-1+ T cells as a potential key immune cell population mediating increased cardiovascular risk in patients with cancer receiving ICI.", "doi": "10.1038/s44161-025-00713-2", "pmid": "41057609", "labels": {"Clinical Genomics Lund": "Service", "Clinical Genomics": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC12520982"}, {"db": "pii", "key": "10.1038/s44161-025-00713-2"}], "notes": [], "created": "2025-11-06T09:28:37.756Z", "modified": "2025-11-06T09:28:38.934Z"}, {"entity": "publication", "iuid": "8822f79ce12c4158bd6128531eaf7657", "links": {"self": {"href": "https://publications.scilifelab.se/publication/8822f79ce12c4158bd6128531eaf7657.json"}, "display": {"href": "https://publications.scilifelab.se/publication/8822f79ce12c4158bd6128531eaf7657"}}, "title": "Kupffer cells dictate hepatic responses to the atherogenic dyslipidemic insult.", "authors": [{"family": "Di Nunzio", "given": "Giada", "initials": "G"}, {"family": "Hellberg", "given": "Sanna", "initials": "S", "orcid": "0000-0003-1791-3693", "researcher": {"href": "https://publications.scilifelab.se/researcher/053fd0cc678f48abb083aaf102f1cec4.json"}}, {"family": "Zhang", "given": "Yuyang", "initials": "Y", "orcid": "0000-0002-3806-6094", "researcher": {"href": "https://publications.scilifelab.se/researcher/d469b9b7fccd4f65a66b2cb87939a157.json"}}, {"family": "Ahmed", "given": "Osman", "initials": "O", "orcid": "0000-0002-2854-2552", "researcher": {"href": "https://publications.scilifelab.se/researcher/fb219b9efad046f6badae392587f62b1.json"}}, {"family": "Wang", "given": "Jiawen", "initials": "J"}, {"family": "Zhang", "given": "Xueming", "initials": "X"}, {"family": "Bj\u00f6rck", "given": "Hanna M", "initials": "HM"}, {"family": "Chizh", "given": "Veronika", "initials": "V"}, {"family": "Schipper", "given": "Ruby", "initials": "R"}, {"family": "Aulin", "given": "Hanna", "initials": "H"}, {"family": "Francis", "given": "Roy", "initials": "R"}, {"family": "Fagerberg", "given": "Linn", "initials": "L", "orcid": "0000-0003-0198-7137", "researcher": {"href": "https://publications.scilifelab.se/researcher/e8db0663a10a4d9e9241457609d5952e.json"}}, {"family": "Gister\u00e5", "given": "Anton", "initials": "A", "orcid": "0000-0002-4614-8030", "researcher": {"href": "https://publications.scilifelab.se/researcher/3e2beec3559745a6ba1859252df4a547.json"}}, {"family": "Metso", "given": "Jari", "initials": "J"}, {"family": "Manf\u00e9", "given": "Valentina", "initials": "V"}, {"family": "Franco-Cereceda", "given": "Anders", "initials": "A"}, {"family": "Eriksson", "given": "Per", "initials": "P"}, {"family": "Jauhiainen", "given": "Matti", "initials": "M"}, {"family": "Hagberg", "given": "Carolina E", "initials": "CE", "orcid": "0000-0002-5497-2855", "researcher": {"href": "https://publications.scilifelab.se/researcher/66bbd07c59044b279527c75f12cd4c04.json"}}, {"family": "Olofsson", "given": "Peder S", "initials": "PS", "orcid": "0000-0003-3473-5948", "researcher": {"href": "https://publications.scilifelab.se/researcher/527d940eee82480bae882e2c8b4af99f.json"}}, {"family": "Malin", "given": "Stephen G", "initials": "SG", "orcid": "0000-0001-7723-9579", "researcher": {"href": "https://publications.scilifelab.se/researcher/86c05018e1e9477181eb7aa86faef7d1.json"}}], "type": "journal article", "published": "2024-03-00", "journal": {"title": "Nat Cardiovasc Res", "issn": "2731-0590", "volume": "3", "issue": "3", "pages": "356-371", "issn-l": null}, "abstract": "Apolipoprotein-B (APOB)-containing lipoproteins cause atherosclerosis. Whether the vasculature is the initially responding site or if atherogenic dyslipidemia affects other organs simultaneously is unknown. Here we show that the liver responds to a dyslipidemic insult based on inducible models of familial hypercholesterolemia and APOB tracing. An acute transition to atherogenic APOB lipoprotein levels resulted in uptake by Kupffer cells and rapid accumulation of triglycerides and cholesterol in the liver. Bulk and single-cell RNA sequencing revealed a Kupffer-cell-specific transcriptional program that was not activated by a high-fat diet alone or detected in standard liver function or pathological assays, even in the presence of fulminant atherosclerosis. Depletion of Kupffer cells altered the dynamic of plasma and liver lipid concentrations, indicating that these liver macrophages help restrain and buffer atherogenic lipoproteins while simultaneously secreting atherosclerosis-modulating factors into plasma. Our results place Kupffer cells as key sentinels in organizing systemic responses to lipoproteins at the initiation of atherosclerosis.", "doi": "10.1038/s44161-024-00448-6", "pmid": "39196121", "labels": {"NGI Single cell": "Service", "NGI Stockholm (Genomics Production)": "Service", "National Genomics Infrastructure": "Service", "NGI Stockholm (Genomics Applications)": "Service", "Bioinformatics Support, Infrastructure and Training": "Collaborative", "Bioinformatics Support and Infrastructure": "Collaborative", "Bioinformatics Support for Computational Resources": "Service", "Bioinformatics (NBIS)": "Collaborative"}, "xrefs": [{"db": "pmc", "key": "PMC11358021"}, {"db": "pii", "key": "10.1038/s44161-024-00448-6"}], "notes": [], "created": "2024-10-14T13:20:41.587Z", "modified": "2025-02-28T14:16:26.867Z"}, {"entity": "publication", "iuid": "d925c6ce825a4cde96a67489dfcef91f", "links": {"self": {"href": "https://publications.scilifelab.se/publication/d925c6ce825a4cde96a67489dfcef91f.json"}, "display": {"href": "https://publications.scilifelab.se/publication/d925c6ce825a4cde96a67489dfcef91f"}}, "title": "Transforming growth factor-\u03b22 is associated with atherosclerotic plaque stability and lower risk for cardiovascular events.", "authors": [{"family": "Edsfeldt", "given": "Andreas", "initials": "A", "orcid": "0000-0002-2691-9192", "researcher": {"href": "https://publications.scilifelab.se/researcher/b4d8310d9d834bd791b791424774b989.json"}}, {"family": "Singh", "given": "Pratibha", "initials": "P"}, {"family": "Matthes", "given": "Frank", "initials": "F", "orcid": "0000-0002-5115-8831", "researcher": {"href": "https://publications.scilifelab.se/researcher/00f734f5167a4de48f38bcdf5e5765ab.json"}}, {"family": "Tengryd", "given": "Christoffer", "initials": "C"}, {"family": "Cavalera", "given": "Michele", "initials": "M"}, {"family": "Bengtsson", "given": "Eva", "initials": "E"}, {"family": "Dun\u00e9r", "given": "Pontus", "initials": "P"}, {"family": "Volkov", "given": "Petr", "initials": "P"}, {"family": "Karadimou", "given": "Glykeria", "initials": "G"}, {"family": "Gister\u00e5", "given": "Anton", "initials": "A", "orcid": "0000-0002-4614-8030", "researcher": {"href": "https://publications.scilifelab.se/researcher/3e2beec3559745a6ba1859252df4a547.json"}}, {"family": "Orho-Melander", "given": "Marju", "initials": "M", "orcid": "0000-0002-3578-2503", "researcher": {"href": "https://publications.scilifelab.se/researcher/7e54fbe6f0fc4eed93108b382e1b2952.json"}}, {"family": "Nilsson", "given": "Jan", "initials": "J", "orcid": "0000-0002-9752-7479", "researcher": {"href": "https://publications.scilifelab.se/researcher/8777140448bc47f0a7984db3c15c0e23.json"}}, {"family": "Sun", "given": "Jiangming", "initials": "J"}, {"family": "Gon\u00e7alves", "given": "Isabel", "initials": "I", "orcid": "0000-0002-2935-0181", "researcher": {"href": "https://publications.scilifelab.se/researcher/53cb42ac6ae8458ea9aaaa1dec1717d9.json"}}], "type": "journal article", "published": "2023-09-05", "journal": {"title": "Cardiovasc. Res.", "issn": "1755-3245", "volume": "119", "issue": "11", "pages": "2061-2073", "issn-l": "0008-6363"}, "abstract": "Transforming growth factor-beta (TGF-\u03b2) exists in three isoforms TGF-\u03b21, -\u03b22, and -\u03b23. TGF-\u03b21 has been suggested to be important for maintaining plaque stability, yet the role of TGF-\u03b22 and -\u03b23 in atherosclerosis remains to be investigated.This study explores the association of the three isoforms of TGF-\u03b2 with plaque stability in the human atherosclerotic disease.\n\nTGF-\u03b21, -\u03b22, and -\u03b23 proteins were quantified in 223 human carotid plaques by immunoassays. Indications for the endarterectomy were: symptomatic carotid plaque with stenosis >70% or without symptoms and >80% stenosis. Plaque mRNA levels were assessed by RNA sequencing. Plaque components and extracellular matrix were measured histologically and biochemically. Matrix metalloproteinases and monocyte chemoattractant protein-1 (MCP-1) was measured with immunoassays. The effect of TGF-\u03b22 on inflammation and protease activity was investigated in vitro using THP-1 and RAW264.7 macrophages. Patients were followed longitudinally for cardiovascular (CV) events.TGF-\u03b22 was the most abundant isoform and was increased at both protein and mRNA levels in asymptomatic plaques. TGF-\u03b22 was the main determinant separating asymptomatic plaques in an Orthogonal Projections to Latent Structures Discriminant Analysis. TGF-\u03b22 correlated positively to features of plaque stability and inversely to markers of plaque vulnerability. TGF-\u03b22 was the only isoform inversely correlated to the matrix-degrading matrix metalloproteinase-9 and inflammation in the plaque tissue. In vitro, TGF-\u03b22 pre-treatment reduced MCP-1 gene and protein levels as well as matrix metalloproteinase-9 gene levels and activity. Patients with plaques with high TGF-\u03b22 levels had a lower risk to suffer from future CV events.\n\nTGF-\u03b22 is the most abundant TGF-\u03b2 isoform in human plaques and may maintain plaque stability by decreasing inflammation and matrix degradation.", "doi": "10.1093/cvr/cvad079", "pmid": "37200403", "labels": {"Affinity Proteomics Uppsala": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC10478752"}, {"db": "pii", "key": "7170345"}], "notes": [], "created": "2023-11-29T19:15:20.896Z", "modified": "2023-11-29T19:15:21.043Z"}]}