{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T05:07:49Z","timestamp":1789708069034,"version":"4.0.1"},"reference-count":77,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T00:00:00Z","timestamp":1789689600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>ADAMTS13 is conventionally regarded as the protease whose severe deficiency causes thrombotic thrombocytopenic purpura (TTP). By cleaving shear-unfolded ultra-large and high-molecular-weight von Willebrand factor (VWF), ADAMTS13 limits a platelet- and leukocyte-adhesive vascular scaffold. We propose a narrower and testable extension of this biology to cancer: an imbalance between VWF burden and ADAMTS13 processing capacity may act as a context-dependent modifier or amplifier of thromboinflammation in selected VWF-rich, shear-exposed tumor vascular niches, but is not established as an initiating or universally rate-limiting cause of cancer-associated thrombosis. We define \u201crelative ADAMTS13 insufficiency\u201d as a research phenotype rather than a diagnosis or evidence of causality. It refers to ADAMTS13 activity outside the severe-deficiency range, typically \u226510%, together with increased VWF burden and a disproportionately low ADAMTS13 activity\/VWF antigen ratio (ADAMTS13:Act\/VWF: Ag). This phenotype is mechanistically nonspecific and may reflect increased VWF release, impaired whole-molecule VWF clearance, reduced ADAMTS13 production, stability, or availability, functional inhibition of proteolysis, reduced VWF susceptibility to cleavage, or shared upstream inflammation. Human evidence from COVID-19 and cancer remains predominantly associative, whereas tumor-relevant perturbation studies provide preclinical causal support in defined models. The causal importance of the VWF\u2013ADAMTS13 axis in human tumors nevertheless remains unproven. We therefore position this module within a broader thromboinflammatory network that includes complement activation, neutrophil extracellular traps, platelet activation, and tissue factor\u2013thrombin\u2013fibrin pathways. ICI-associated endothelial phenotypes are distinguished from rare ICI-associated immune TTP with categorical severe ADAMTS13 deficiency. Candidate interventions are accordingly presented as mechanistic research nodes requiring staged validation rather than as established oncology therapies.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1922929","type":"journal-article","created":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T04:31:18Z","timestamp":1789705878000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["ADAMTS13 as a thromboinflammatory brake at the vascular-immune interface: from viral immunothrombosis to the tumor microenvironment"],"prefix":"10.3389","volume":"17","author":[{"given":"Peng","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Interventional Oncology, Zibo Central Hospital","place":["Zibo, Shandong, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoyu","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Pathology, Zibo Central Hospital","place":["Zibo, Shandong, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Peng","sequence":"additional","affiliation":[{"name":"Department of Pathology, Zibo Central Hospital","place":["Zibo, Shandong, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Tian","sequence":"additional","affiliation":[{"name":"Department of Oncology, Zibo Central Hospital","place":["Zibo, Shandong, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,18]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2025.3807","article-title":"Immune thrombotic thrombocytopenic purpura: a review","volume":"334","author":"Pishko","year":"2025","journal-title":"JAMA"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.3390\/ijms25158137","article-title":"ADAMTS13 in the new era of TTP","volume":"25","author":"Papakonstantinou","year":"2024","journal-title":"Int J Mol Sci"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2011-02-306597","article-title":"Unraveling the scissile bond: how ADAMTS13 recognizes and cleaves von Willebrand factor","volume":"118","author":"Crawley","year":"2011","journal-title":"Blood"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1182\/hematology.2023000501","article-title":"Medical consult: aHUS, TTP? 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