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Static Adhesion Assay for the Study of Integrin Activation in T Lymphocytes
Published on: June 13, 2014
β-1,4-galactosyltransferase-I activates proliferation and participates in intercellular contacts of lymphocytes
Xiaolei Sun1, Yuanyuan Wu2, Ying Wang1
1Department of Immunology, Nantong University, Nantong, Jiangsu, PR China.
Beta-1,4-galactosyltransferase I (β-1,4-GalT-I) mediates several biological mechanisms as a key enzyme in glycobiology, but the role of β-1,4-GalT-I in immune system remains unclear. We conducted experiments to investigate whether β-1,4-GalT-I is participating in the activation of Jurkat T cell and intercellular contacts formed by co-incubation of Jurkat and Raji cells in the presence of the superantigen staphylococcal enterotoxin B (SEB). Jurkat cells were also activated by CD3/CD28 co-stimulation in order to examine the expression pattern and cellular distribution of β-1,4-GalT-I upon stimulation. Here we found that β-1,4-GalT-I expression was enhanced and rearranged on the cell surface of activated Jurkat cells. Further, immunofluorescence staining assays revealed that β-1,4-GalT-I co-aggregated with CD3 and CD28 molecules in the junction sides of Jurkat and SEB pulsed Raji cells. Our study also showed that silencing of β-1,4-GalT-I inhibited Jurkat activated Raji cell conjugations and reduced the proliferation rate of activated Jurkat cells. Our data provide evidence that β-1,4-GalT-I plays a role in activation of Jurkat T lymphocytes and participates in intercellular contact formation.
Beta-1,4-galactosyltransferase I (β-1,4-GalT-I) mediates several biological mechanisms as a key enzyme in glycobiology, but the role of β-1,4-GalT-I in immune system remains unclear. We conducted experiments to investigate whether β-1,4-GalT-I is participating in the activation of Jurkat T cell and intercellular contacts formed by co-incubation of Jurkat and Raji cells in the presence of the superantigen staphylococcal enterotoxin B (SEB). Jurkat cells were also activated by CD3/CD28 co-stimulation in order to examine the expression pattern and cellular distribution of β-1,4-GalT-I upon stimulation. Here we found that β-1,4-GalT-I expression was enhanced and rearranged on the cell surface of activated Jurkat cells. Further, immunofluorescence staining assays revealed that β-1,4-GalT-I co-aggregated with CD3 and CD28 molecules in the junction sides of Jurkat and SEB pulsed Raji cells. Our study also showed that silencing of β-1,4-GalT-I inhibited Jurkat activated Raji cell conjugations and reduced the proliferation rate of activated Jurkat cells. Our data provide evidence that β-1,4-GalT-I plays a role in activation of Jurkat T lymphocytes and participates in intercellular contact formation.
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