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-1,6-n-Acetylglucosaminyltransferase, an Enzyme Essential for Biosynthesis of P-Selectin Ligands1
*
Vascular Research Division, Departments of Pathology, Brigham and Women’s Hospital and Harvard Medical School; and
Department of Immunology and Infectious Diseases, Harvard School of Public Health and Department of Medicine, Harvard Medical School, Boston, MA 02115
TCR activation of naive T cells in the presence of IL-12 drives
polarization toward a Th1 phenotype and synthesis of P- and E-selectin
ligands. Fucosyltransferase VII (Fuc-T VII) and core 2
-1,6-N-acetylglucosaminyltransferase (C2GnT) are
critical for biosynthesis of selectin ligands. P-selectin glycoprotein
ligand-1 is the best characterized ligand for P-selectin and
also binds E-selectin. The contributions of TCR and cytokine signaling
pathways to up-regulate Fuc-T VII and C2GnT during biosynthesis of E-
and P-selectin ligands, such as P-selectin glycoprotein ligand 1, are
unknown. IL-12 signals via the STAT4 pathway. Here, naive DO11.10 TCR
transgenic and STAT4-/- TCR transgenic CD4+ T
cells were stimulated with Ag and IL-12 (Th1 condition), IL-4 (Th2), or
neutralizing anti-IL-4 mAb only (Th0). The levels of Fuc-T VII and
C2GnT mRNA in these cells were compared with their adhesive
interactions with P- and E-selectin in vitro under flow. The data show
IL-12/STAT4 signaling is necessary for induction of C2GnT, but not
Fuc-TVII mRNA, and that STAT4-/- Th1 cells do not traffic
normally to sites of inflammation in vivo, do not interact with
P-selectin, and exhibit a partial reduction of E-selectin interactions
under shear stress in vitro. Ag-specific TCR activation in
CD4+ T cells was sufficient to trigger induction of
Fuc-TVII, but not C2GnT, mRNA and expression of E-selectin, but not
P-selectin, ligands. Thus, Fuc-T VII and C2GnT are regulated by
different signals during Th cell differentiation, and both cytokine and
TCR signals are necessary for the expression of E- and P-selectin
ligands.
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