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        <identifier>oai:figshare.com:article/30729362</identifier>
        <datestamp>2026-09-15T18:25:47Z</datestamp>
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          <dc:title>CITE_seq</dc:title>
          <dc:creator>Cenfu Wei (22694909)</dc:creator>
          <dc:subject>Gastroenterology and hepatology</dc:subject>
          <dc:subject>CITESeq</dc:subject>
          <dc:subject>UC</dc:subject>
          <dc:subject>VDZ</dc:subject>
          <dc:description>&lt;p dir="ltr"&gt;A major barrier to precision medicine for ulcerative colitis (UC) is the inability to predict and mechanistically explain treatment responses. Using daily patient-reported outcomes from a phase 3b comparative trial of 768 participants, we identified four distinct patient response trajectory groups for vedolizumab (anti-integrin) and adalimumab (antitumor necrosis factor) in UC. Validation in a second phase 3 trial of 591 participants linked vedolizumab trajectories to long-term disease complications. Bulk, single-cell, and spatial, transcriptomics and proteomics, identified vascular inflammation to be associated with vedolizumab nonresponse via SPP1+ monocytes and the angiopoetin-2 pathway. In a real-world cohort of 3,187 patients with UC, concomitant use of renin-angiotensin system inhibitors (modulators of vascular inflammation and angiopoietin-2 signaling) was associated with reduced long-term complications for vedolizumab but not anti-cytokine therapies. These findings define a response trajectory-based taxonomy, and endotype-specific outcome prediction, implicating vascular inflammation as a drug-specific and targetable resistance pathway for vedolizumab in UC.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-15T18:25:47Z</dc:date>
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          <dc:identifier>10.6084/m9.figshare.30729362.v1</dc:identifier>
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