Activity and secretion of sialyltransferase in primary monolayer cultures of rat hepatocytes cultured with and without dexamethasone

W, van Dijk; Boers, W.; Sala, Mieke; Am, Lasthuis; Mookerjea, Sailen

doi:10.1139/o86-014

Cited by 28 publications

(1 citation statement)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The existence of sialyltransferases within the extracellular milieau, particularly the blood, has been known for quite some time. Upregulation of serum ST6GAL1 during inflammation was attributed to the induction of hepatic expression, leading to the designation of ST6GAL1 as an acute phase reactant (Kaplan et al, 1983; Jamieson et al, 1993; Jamieson et al, 1987; Jamieson, 1988; van Dijk et al, 1986). However, it was also recognized that in addition to hepatocytes, B cells are sophisticated expressers of ST6GAL1 , utilizing multiple tissue-specific transcripts during development (Wuensch et al, 2000; Wang et al, 1993; Lo and Lau, 1996).…”

Section: Discussionmentioning

confidence: 99%

B cells suppress medullary granulopoiesis by an extracellular glycosylation-dependent mechanism

Irons

Lee‐Sundlov

Zhu

et al. 2019

eLife

View full text Add to dashboard Cite

The immune response relies on the integration of cell-intrinsic processes with cell-extrinsic cues. During infection, B cells vacate the marrow during emergency granulopoiesis but return upon restoration of homeostasis. Here we report a novel glycosylation-mediated crosstalk between marrow B cells and hematopoietic progenitors. Human B cells secrete active ST6GAL1 sialyltransferase that remodels progenitor cell surface glycans to suppress granulopoiesis. In mouse models, ST6GAL1 from B cells alters the sialylation profile of bone marrow populations, and mature IgD+ B cells were enriched in sialylated bone marrow niches. In clinical multiple myeloma, ST6GAL1 abundance in the multiple myeloma cells negatively correlated with neutrophil abundance. These observations highlight not only the ability of medullary B cells to influence blood cell production, but also the disruption to normal granulopoiesis by excessive ST6GAL1 in malignancy.

show abstract