ArticleFrontiers in immunology2026
Loss of ST8Sia6 mediated α-2,8-linked di-sialylation enhances T cell-dependent antibody responses and promotes autoimmunity in aged mice.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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Who cites it
1 citing paper in PubMed.
- Loss of ST8SIA6 is associated with enhanced MUC16-Integrin β4 signaling and aggressive phenotypes in colorectal cancer.Biochemistry and biophysics reports · 2026Article
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9 authors.
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Abstract
Introduction: Sialic acids are terminal nine-carbon sugars that form sialoglycans on the glycocalyx of all vertebrate cell surfaces. In this exposed position, they fulfill various functions in the immune system, including involvement in host-pathogen interactions and control of immune cell activation. The synthesis of sialoglycans is catalyzed by sialyltransferases. One of these is ST8Sia6, which is known to catalyze the synthesis of α-2,8-linked di-sialyl motifs and to be upregulated in plasma cells. Methods: We studied the role of ST8Sia6 in the immune system by examining a Results: The Discussion: These results demonstrate that the loss of ST8Sia6-mediated α-2,8-linked di-sialylation enhances T cell-dependent immune responses and promotes an accumulation of strongly activated B cells and an autoimmune-like phenotype upon aging.
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