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.