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However, allo\u2010HSCT is associated with significant complications. The most common and debilitating among them is graft\u2010versus\u2010host disease (GVHD). In GVHD, donor\u2010derived T cells mount an alloimmune response against the recipient. The alloimmune response involves several steps, including recognition of recipient antigens, activation and proliferation of T cells in secondary lymphoid organs, and homing into GVHD\u2010targeted organs. Adhesion molecules on T cells and endothelial cells mediate homing of T cells into lymphoid and non\u2010lymphoid tissues. In this study, we showed that Von Willebrand factor (VWF), an adhesion molecule secreted by activated endothelial cells, plays an important role in mouse models of GVHD. We investigated the effect of the VWF\u2010cleaving protease ADAMTS13 on GVHD. We found that ADAMTS13 reduced the severity of GVHD after bone marrow transplantation from C57BL6 donor to BALB\/C recipient mice. A recombinant VWF\u2010A2 domain peptide also reduced GVHD in mice. We showed that ADAMTS13 and recombinant VWF\u2010A2 reduced the binding of T cells to endothelial cells and VWF in\u00a0vitro, and reduced the number of T cells in lymph nodes, Peyer's patches and GVHD\u2010targeted organs in\u00a0vivo. We identified LFA\u20101 (\u03b1L\u03b22) as the binding site of VWF on T cells. Our results showed that blocking T\u2010cell homing by ADAMTS13 or VWF\u2010A2 peptide reduced the severity of the GVHD after allo\u2010HSCT, a potentially novel method for treating and preventing GVHD.<\/jats:p>","DOI":"10.1111\/jcmm.18457","type":"journal-article","created":{"date-parts":[[2024,7,4]],"date-time":"2024-07-04T10:26:23Z","timestamp":1720088783000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["The effect of <scp>ADAMTS13<\/scp> on graft\u2010versus\u2010host disease"],"prefix":"10.1111","volume":"28","author":[{"given":"Dan","family":"Li","sequence":"first","affiliation":[{"name":"Department of Hematopoietic Biology &amp; Malignancy The University of Texas MD Anderson Cancer Center  Houston Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9992-8356","authenticated-orcid":false,"given":"Min Soon","family":"Cho","sequence":"additional","affiliation":[{"name":"Section of Benign Hematology The University of Texas MD Anderson Cancer Center  Houston Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-2122-0527","authenticated-orcid":false,"given":"Ricardo","family":"Gonzalez\u2010Delgado","sequence":"additional","affiliation":[{"name":"Section of Benign Hematology The University of Texas MD Anderson Cancer Center  Houston Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaowen","family":"Liang","sequence":"additional","affiliation":[{"name":"Department of Integrative Biology and Pharmacology McGovern Medical School, The University of Texas Health Science Center  Houston Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing\u2010Fei","family":"Dong","sequence":"additional","affiliation":[{"name":"Bloodworks Research Institute and Hematology Division, Department of Medicine University of Washington School of Medicine  Seattle Washington USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miguel A.","family":"Cruz","sequence":"additional","affiliation":[{"name":"Center for Translational Research on Inflammatory Diseases (CTRID), Michael E. 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