SIGLEC10 is a sialic acid-binding inhibitory receptor that functions as an innate immune checkpoint regulating immune cell activation. The protein mediates sialic acid-dependent cell adhesion and acts as an inhibitory receptor through ligand-induced tyrosine phosphorylation, recruiting cytoplasmic phosphatase PTPN6/SHP-1 via SH2 domain interactions to block signal transduction 1. SIGLEC10 negatively regulates B cell antigen receptor signaling and, in association with CD24, suppresses immune responses to danger-associated molecular patterns 2. The CD24/SIGLEC10 axis represents a critical innate immune checkpoint in cancer immunotherapy; tumor-expressed CD24 interacts with SIGLEC10 on tumor-associated macrophages to promote immune evasion by inhibiting macrophage phagocytosis 1. Blockade of CD24-SIGLEC10 interaction using monoclonal antibodies or genetic ablation enhances tumor phagocytosis and reduces tumor growth in ovarian and breast cancers 1. In hematological malignancies, the CD24/SIGLEC-10 axis is identified as a major "don't eat me" signal comparable to CD47/SIRPα and PD-1/PD-L1 pathways 3. Additionally, CD52-SIGLEC10 interactions between chemoresistant leukemic cells and monocytes may contribute to immune evasion in relapsed/refractory AML 4. Emerging therapeutic strategies include CD24-targeted monoclonal antibodies and nano-LYTAC systems for CD24 degradation to restore macrophage phagocytic function 5. Disease associations also extend to neurodegenerative conditions, with elevated SIGLEC10 expression identified as a potential diagnostic biomarker for Alzheimer's disease 6.