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Sialoadhesin ligand expression identifies a subset of CD4+ Foxp32 T cells with a distinct activation and glycosylation profile

Journal of Immunology, ISSN: 0022-1767, Vol: 190, Issue: 6, Page: 2593-2602
2013
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Sialoadhesin (Sn) is a sialic acid-binding Ig-like lectin expressed selectively on macrophage subsets. In a model of experimental autoimmune encephalomyelitis, Sn interacted with sialylated ligands expressed selectively on CD4Foxp3 regulatory T cells (Tregs) and inhibited their proliferation. In this study, we examined the induction of Sn ligands (SnL) on all splenic CD4 T cells following in vitro activation. Most CD4 Tregs strongly upregulated SnL, whereas only a small subset of ∼20% CD4 Foxp32 T cells (effector T cells [Teffs]) upregulated SnL. SnL Teffs displayed higher levels of activation markers CD25 and CD69, exhibited increased proliferation, and produced higher amounts of IL-2 and IFN-γ than corresponding SnL2 Teffs. Coculture of activated Teffs with Sn macrophages or Sn Chinese hamster ovary cells resulted in increased cell death, suggesting a regulatory role for Sn-SnL interactions. The key importance of a2,3-sialylation in SnL expression was demonstrated by increased binding of a2,3-linkage-specific Maackia amurensis lectin, increased expression of a2,3-sialyltransferase ST3GalVI, and loss of SnL following treatment with an a2,3-linkage-specific sialidase. The induction of SnL on activated CD4 T cells was dependent on N-glycan rather than O-glycan biosynthesis and independent of the mucin-like molecules CD43 and P-selectin glycoprotein ligand-1, previously implicated in Sn interactions. Induction of ligands on CD4Foxp32 Teffs was also observed in vivo using the New Zealand Black 3 New Zealand White F1 murine model of spontaneous lupus and SnL levels on Teffs correlated strongly with the degree of proteinuria. Collectively, these data indicate that SnL is a novel marker of activated CD4 Teffs that are implicated in the pathogenesis of autoimmune diseases. © 2013 by The American Association of Immunologists, Inc.

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