{"entity": "researcher", "timestamp": "2026-08-15T22:41:17.812Z", "family": "Stritt", "given": "Simon", "initials": "S", "orcid": "0000-0002-4299-4934", "affiliations": ["Department of Immunology, Genetics and Pathology, Uppsala University , Uppsala, Sweden."], "links": {"self": {"href": "https://publications.scilifelab.se/researcher/b561f8d6fb1a46d0ae76c66e440956a1.json"}, "display": {"href": "https://publications.scilifelab.se/researcher/b561f8d6fb1a46d0ae76c66e440956a1"}}, "publications": [{"entity": "publication", "iuid": "4371a4380e6d4e3294f5c4116411dd13", "links": {"self": {"href": "https://publications.scilifelab.se/publication/4371a4380e6d4e3294f5c4116411dd13.json"}, "display": {"href": "https://publications.scilifelab.se/publication/4371a4380e6d4e3294f5c4116411dd13"}}, "title": "Immune-interacting lymphatic endothelial subtype at capillary terminals drives lymphatic malformation.", "authors": [{"family": "Petkova", "given": "Milena", "initials": "M", "orcid": "0000-0002-7186-7256", "researcher": {"href": "https://publications.scilifelab.se/researcher/458b9dbc408c4118b97be343da8b3b49.json"}}, {"family": "Kraft", "given": "Marle", "initials": "M", "orcid": "0000-0002-3523-7003", "researcher": {"href": "https://publications.scilifelab.se/researcher/6bac6d144f4143b7ad9ad0a9058d95a0.json"}}, {"family": "Stritt", "given": "Simon", "initials": "S", "orcid": "0000-0002-4299-4934", "researcher": {"href": "https://publications.scilifelab.se/researcher/b561f8d6fb1a46d0ae76c66e440956a1.json"}}, {"family": "Martinez-Corral", "given": "Ines", "initials": "I", "orcid": "0000-0001-9194-2412", "researcher": {"href": "https://publications.scilifelab.se/researcher/0f961131890c4422b8ce5a5d2d1f1dc9.json"}}, {"family": "Orts\u00e4ter", "given": "Henrik", "initials": "H", "orcid": "0000-0002-4046-4702", "researcher": {"href": "https://publications.scilifelab.se/researcher/1f597cc7c8104728ae168db36a8ee9e7.json"}}, {"family": "Vanlandewijck", "given": "Michael", "initials": "M", "orcid": "0000-0002-0709-7808", "researcher": {"href": "https://publications.scilifelab.se/researcher/aa2148fbafb44d59bd110e36bd77769c.json"}}, {"family": "Jakic", "given": "Bojana", "initials": "B", "orcid": "0000-0002-2339-5928", "researcher": {"href": "https://publications.scilifelab.se/researcher/31f0bb6137144060a45a40650aacadc7.json"}}, {"family": "Baselga", "given": "Eul\u00e0lia", "initials": "E", "orcid": "0000-0003-1086-8439", "researcher": {"href": "https://publications.scilifelab.se/researcher/12b835a79f01492e82d1280c8050e01b.json"}}, {"family": "Castillo", "given": "Sandra D", "initials": "SD", "orcid": "0000-0002-7007-3155", "researcher": {"href": "https://publications.scilifelab.se/researcher/de3d0367a9d8474197f66365c1b5c040.json"}}, {"family": "Graupera", "given": "Mariona", "initials": "M", "orcid": "0000-0003-4608-4185", "researcher": {"href": "https://publications.scilifelab.se/researcher/76ead57229884f90bff307099a9a70ea.json"}}, {"family": "Betsholtz", "given": "Christer", "initials": "C", "orcid": "0000-0002-8494-971X", "researcher": {"href": "https://publications.scilifelab.se/researcher/a00cfe9d521047f280978d84d7dcf1b3.json"}}, {"family": "M\u00e4kinen", "given": "Taija", "initials": "T", "orcid": "0000-0002-9338-1257", "researcher": {"href": "https://publications.scilifelab.se/researcher/bf99a0589d1f4532b532bfc575edaada.json"}}], "type": "journal article", "published": "2023-04-03", "journal": {"title": "J. Exp. Med.", "issn": "1540-9538", "volume": "220", "issue": "4", "issn-l": "0022-1007"}, "abstract": "Oncogenic mutations in PIK3CA, encoding p110\u03b1-PI3K, are a common cause of venous and lymphatic malformations. Vessel type-specific disease pathogenesis is poorly understood, hampering development of efficient therapies. Here, we reveal a new immune-interacting subtype of Ptx3-positive dermal lymphatic capillary endothelial cells (iLECs) that recruit pro-lymphangiogenic macrophages to promote progressive lymphatic overgrowth. Mouse model of Pik3caH1047R-driven vascular malformations showed that proliferation was induced in both venous and lymphatic ECs but sustained selectively in LECs of advanced lesions. Single-cell transcriptomics identified the iLEC population, residing at lymphatic capillary terminals of normal vasculature, that was expanded in Pik3caH1047R mice. Expression of pro-inflammatory genes, including monocyte/macrophage chemokine Ccl2, in Pik3caH1047R-iLECs was associated with recruitment of VEGF-C-producing macrophages. Macrophage depletion, CCL2 blockade, or anti-inflammatory COX-2 inhibition limited Pik3caH1047R-driven lymphangiogenesis. Thus, targeting the paracrine crosstalk involving iLECs and macrophages provides a new therapeutic opportunity for lymphatic malformations. Identification of iLECs further indicates that peripheral lymphatic vessels not only respond to but also actively orchestrate inflammatory processes.", "doi": "10.1084/jem.20220741", "pmid": "36688917", "labels": {"Bioinformatics Support and Infrastructure": "Service", "Bioinformatics Support, Infrastructure and Training": "Service", "Bioinformatics Support for Computational Resources": "Service", "Bioinformatics (NBIS)": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC9884640"}, {"db": "pii", "key": "213817"}], "notes": [], "created": "2023-11-16T12:40:26.995Z", "modified": "2024-01-16T13:48:33.714Z"}]}