ArticleFrontiers in immunology2026
Enhanced sialylation of bone marrow mesenchymal stromal cells contributes to immune remodeling through macrophage polarization in multiple myeloma patients.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: In multiple myeloma (MM), the immune system is disrupted, partly due to tumor-modified bone marrow mesenchymal stromal cells (BM-MSCs). These MSCs show altered glycosylation, including increased sialylation, which may promote immune evasion through Siglec interactions. Methods: We quantified sialic acids and Siglec ligands on healthy donors-, MM-, T-MM-(treated multiple myeloma) and MGUS (monoclonal gammopathy of undetermined significance)-MSCs, and examined how different culture conditions (myeloma coculture, conditioned medium, hypoxia, inflammation, 3D culture) affect MSC glycosylation. Expression of 84 glycosylation-related genes was screened by qPCR. Macrophage polarization was then assessed after modulating MSC sialylation using inhibitors or an activator. Results: MM-MSCs exhibited significantly higher surface sialylation than HD-, T-MM-, and MGUS-MSCs. MM-MSC sialylation was positively correlated with the percentage of plasma cells and the LDH levels of MM patients. Direct MSC-plasma cell cocultures further enhanced hypersialylation compared with conditioned medium or transwell coculture, indicating a contact-dependent mechanism. qPCR screening identified two dysregulated genes, ST6Gal1 and NEU2, implicated in the sialylation pathway. Inflammation and hypoxia appeared as key players in the expression of Siglec-7L, Siglec-9L and ST6Gal1 by MSCs. Functionally, we showed that increased sialylation promoted an M2-like phenotype as measured by CD206, whereas inhibition shifted macrophages toward an M1-like profile as measured by CD40 and HLA-DR. We also showed that when MSC sialylation is inhibited, their ability to induce an M2 phenotype is reduced, as evidenced by the lower production of M2-associated cytokines. Conclusion: Our findings suggest that BM-MSC hypersialylation may contribute to immune remodeling in MM.
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