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        <datestamp>2026-10-01T12:15:11Z</datestamp>
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          <dc:title>Image 2_Spatial immune ecosystems and therapy resistance in large B-cell lymphoma: from single-cell multi-omics to immunotherapy-matched validation.tiff</dc:title>
          <dc:creator>Gaojie Liu (9133553)</dc:creator>
          <dc:creator>Junwei Yang (112231)</dc:creator>
          <dc:creator>Han Li (10885)</dc:creator>
          <dc:creator>Lishuo Deng (25152123)</dc:creator>
          <dc:creator>Liuxin Jiang (25152120)</dc:creator>
          <dc:creator>Yuetong Tan (25152126)</dc:creator>
          <dc:creator>Jianxiong Zhu (5321027)</dc:creator>
          <dc:creator>Jifan Li (6498407)</dc:creator>
          <dc:creator>Yao Wang (102387)</dc:creator>
          <dc:subject>Genetic Immunology</dc:subject>
          <dc:subject>antibody-drug conjugates</dc:subject>
          <dc:subject>bispecific antibodies</dc:subject>
          <dc:subject>cancer immunotherapy</dc:subject>
          <dc:subject>CAR-T cells</dc:subject>
          <dc:subject>diffuse large B-cell lymphoma</dc:subject>
          <dc:subject>large B-cell lymphoma</dc:subject>
          <dc:subject>pathology-ready biomarkers</dc:subject>
          <dc:subject>spatial immunology</dc:subject>
          <dc:description>&lt;p&gt;Large B-cell lymphomas, particularly diffuse large B-cell lymphoma (DLBCL), provide a clinically important model in which tumor-intrinsic programs, immune recognition, effector-cell fitness, and tissue architecture jointly shape response and resistance to immunotherapy. Although molecular classification has refined the understanding of lymphoma biology, relapse after chemoimmunotherapy, chimeric antigen receptor (CAR) T-cell therapy, CD20×CD3 bispecific antibodies, antibody-drug conjugates (ADCs), and immune-combination strategies cannot be explained by genetics or target-antigen expression alone. Single-cell and spatial multi-omics now allow lymphoma to be interpreted as a spatial immune ecosystem composed of malignant B-cell states, exhausted or regulatory T-cell programs, myeloid suppressive hubs, stromal and vascular compartmentalization, metabolic gradients, and local communication networks. This Review synthesizes recent DLBCL and large B-cell lymphoma ecosystem studies from a cancer-immunology perspective, emphasizing how spatial immune organization may influence effector access, antigen engagement, macrophage-mediated suppression, antibody exposure, and treatment-associated spatial change. We propose a treatment-matched validation framework that connects high-dimensional discovery to formalin-fixed paraffin-embedded (FFPE)-compatible pathology assays, including reduced marker panels for CAR T-cell therapy, bispecific antibodies, ADC-containing therapy, and immune-combination trials. Throughout, we distinguish observed tissue organization from computationally inferred communication and experimentally validated mechanisms. The resulting framework is intended as a trial-design and biomarker-development roadmap, not as a current clinical allocation algorithm.&lt;/p&gt;</dc:description>
          <dc:date>2026-10-01T12:15:11Z</dc:date>
          <dc:type>Image</dc:type>
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          <dc:identifier>10.3389/fimmu.2026.1916056.s003</dc:identifier>
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          <dc:rights>CC BY 4.0</dc:rights>
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