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(1,3)-Fucosyltransferase VII in Activated CD4+ T Cells by TGF-ß1 Through a p38 Mitogen-Activated Protein Kinase-Dependent Pathway1
Department of Microbiology-Immunology, Northwestern University Medical School, Chicago, IL 60611
Homing of effector T cells to sites of inflammation, particularly
in the skin, is dependent on T cell expression of ligands for the
endothelial selectins. Underlying expression of these ligands is the
expression of 
(1,3)-fucosyltransferase VII (FucT-VII), a FucT
essential for biosynthesis of selectin ligands. FucT-VII is sharply
induced in activated T cells by IL-12, but cytokines other than IL-12
that induce FucT-VII and functional selectin ligands have not been
identified, and are likely to be important in homing of T cells to
other selectin-dependent sites. Screening of a number of cytokines
known to be active on T cells identified only TGF-ß1 as able to
up-regulate FucT-VII mRNA levels and selectin ligands on activated CD4
T cells. The sharp increase in FucT-VII induced by TGF-ß1 in
activated T cells was completely blocked by pharmacologic inhibition of
p38 mitogen-activated protein kinase, but was unaffected by
mitogen-activated protein/extracellular signal-related kinase kinase
inhibitors. The selective ability of TGF-ß1 to induce selectin
ligands on activated T cells is likely important for T cell homing to
the gut, which is a strongly selectin-dependent site, and correlates
with the ability of TGF-ß1 to coordinately induce other
gut-associated homing pathways.
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