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CUTTING EDGE |

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Department of Microbiology-Immunology, Northwestern University Medical School, Chicago, IL 60611; and
Department of Microbiology and Immunology and the Walther Oncology Center, Indiana University School of Medicine, Indianapolis, IN 46202
A role for Stat4 in IL-12-induced up-regulation of selectin
ligands on Th1 cells was explored. Th1 cells generated from
Stat4-/- mice exhibited no IL-12-inducible P-selectin
ligands, no up-regulation of core 2
1,6-glucosaminyltransferase I
(C2GlcNAcT-I), and low levels of the Th1 transcription factor T-bet. In
contrast, Stat4-/- Th1 cells exhibited only a partial
defect in expression of IL-12-inducible E-selectin ligands and
expressed equivalently high levels of
1,3-fucosyltransferase VII
(FucT-VII) as wild-type Th1 cells. FucT-VII expression was induced by T
cell activation, and was enhanced by IL-12 independently of Stat4,
whereas C2GlcNAcT-I up-regulation was mediated exclusively by IL-12,
acting through Stat4. These data show that FucT-VII and C2GlcNAcT-I are
controlled through distinct pathways and imply the existence of at
least one other IL-12-inducible glycosyltransferase required for
E-selectin and possibly P-selectin ligand formation in Th1
cells.
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