{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nVISTA (also known as VSIR) is a novel inhibitory immune checkpoint molecule that plays a critical role in maintaining immune homeostasis. It is constitutively expressed on naïve T cells and is highly enriched in cells of the myeloid lineage—including monocytes, macrophages, dendritic cells, and granulocytes—where it restrains T‐cell activation and thereby promotes peripheral tolerance. Unique structural features in its extracellular immunoglobulin–like domain (such as additional disulfide bonds and specialized loop regions) underpin its ability to engage binding partners (e.g. PSGL‐1 at acidic pH and VSIG‐3) to transmit inhibitory signals."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn numerous tumor microenvironments—including pancreatic, melanoma, lung, colorectal, ovarian and other cancers—VISTA is frequently upregulated, predominantly on tumor‐infiltrating immune cells such as macrophages and myeloid‐derived suppressor cells. This upregulation contributes to an immunosuppressive milieu that can impair anti–tumor T-cell responses and, in some settings, mediate resistance to existing checkpoint blockers (e.g. anti–PD-1/PD-L1 therapies). Moreover, studies in patient samples have correlated VISTA expression with distinct clinicopathologic features and survival outcomes—findings that vary with tumor type, reflecting its complex role as both a biomarker and a mediator of immune escape."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nTherapeutically, targeting the VISTA pathway—either alone or in combination with other checkpoint inhibitors—offers a promising strategy to overcome immune resistance in cancer. Preclinical investigations have shown that blockade of VISTA can reverse myeloid‐mediated T-cell suppression, enhance cytotoxic lymphocyte responses, and synergize with other therapies (including agents disrupting STAT3–driven transcriptional regulation) to improve tumor control. 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