{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSiglec‐1 (CD169) is a type I interferon–inducible, sialic acid–binding lectin predominantly expressed on myeloid cells such as dendritic cells and macrophages. It plays a pivotal role in host–pathogen interactions by recognizing sialylated gangliosides (for example, GM3) on the membranes of enveloped viruses. This recognition facilitates both the capture of viruses—including human immunodeficiency virus type 1 (HIV‐1) and severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‑2)—and their subsequent sequestration in non‐lysosomal compartments, thereby promoting trans‐infection of lymphocytes. In addition, Siglec‐1 on virus‐exposed dendritic cells has been shown to influence downstream cytokine responses and even modulate innate antiviral signals."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in viral capture and dissemination, Siglec‐1 expressed on lymph node sinus and tissue‐resident macrophages functions as an important modulator of immune responses in cancer and autoimmunity. High densities of Siglec‐1–positive macrophages in tumors and regional lymph nodes correlate with enhanced infiltration of cytotoxic T cells and, in some studies, with favorable clinical outcomes, suggesting a co‐stimulatory role in antitumor immunity. In parallel, elevated expression levels of Siglec‐1 have been documented in inflammatory and autoimmune settings—including rheumatoid arthritis, pediatric systemic lupus erythematosus, multiple sclerosis, and idiopathic inflammatory myopathies—where it serves as a surrogate marker for an activated type I interferon signature and overall disease activity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nGenetic and translational studies further underscore the multifaceted role of Siglec‐1. Notably, loss‐of‐function variants in SIGLEC1 result in measurable deficits in viral capture and trans‐infection ex vivo, although such variants do not appear to significantly alter overall HIV‐1 disease progression in vivo. In addition, differential expression of Siglec‐1 in the lymphatic endothelium and its involvement in extracellular vesicle uptake and antigen presentation point to new therapeutic avenues for modulating immune responses in infectious as well as inflammatory conditions—for instance, in mitigating the extrapulmonary dissemination of Mycobacterium tuberculosis. Comprehensive reviews highlight Siglec‐1’s unique structure, with extended immunoglobulin–like domains, which underpins its ability to bind a wide array of sialylated ligands and to contribute to both pathogen dissemination and immunoregulation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "33", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Nuria Izquierdo-Useros, Maier Lorizate, Maria C Puertas, et al. 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