Introduction
Fucosylation is a biological process that involves the transfer of a
fucose residue to oligosaccharide chains carried by cell-surface
glycoproteins or glycolipids, and is regulated by fucosyltransferases
(FUTs) (1). Depending on the site of the oligosaccharide chain to which
the fucose is added, fucosylation is categorized into two types, core
fucosylation and terminal fucosylation, which are mediated by different
FUTs. These fucosylated carbohydrate moieties play a crucial role in
regulating various biological processes within cells, including cell
survival, adhesion, cellular signaling and function, and cell-to-cell or
cell-to-environment interactions. In effect, recent research has
revealed that altered fucosylation in cells and tissues is associated
with a number of diseases, ranging from inflammatory conditions such as
collagen-induced arthritis (2), rheumatoid arthritis (3, 4), allergic
airway inflammation (5), bacterial intestinal inflammation (6) and dry
eye disease (7) to multiple types of cancers (8).
In our previous study (7), we observed increased inflammatory responses
on the ocular surface and activation of CD4 T cells in Fut1knockout (KO) mice with a deficiency in terminal fucosylation mediated
by FUT1, resulting in a dry eye disease phenotype. While the role of
FUT1-mediated fucosylation has been previously investigated in vascular
endothelial cells (3, 9) and synovial fibroblasts at the cellular level
(4), its effects on immune cells and their interactions with T cells
remain unclear. Therefore, in this current study, we analyzed the
transcriptome profiles of splenocytes in Fut1 KO mice compared to
wild-type (WT) mice, and investigated the impact of these profiles on T
cell proliferation and differentiation.