Splenocytes with fucosylation deficiency promote T cell proliferation
and differentiation through thrombospondin-1 downregulation
Abstract
Fucosylation plays a critical role in cell-to-cell interactions and
disease progression. However, the effects of fucosylation on splenocytes
and their interactions with T cells remain unclear. In this study, we
aimed to explore the transcriptome profiles of splenocytes deficient in
fucosyltransferase (FUT) 1, an enzyme that mediates fucosylation, and
investigate their impact on the proliferation and differentiation of T
cells. We analyzed and compared the transcriptomes of splenocytes
isolated from Fut1 knockout (KO) mice and those from wild-type
(WT) mice using RNA-seq. Additionally, we examined the effects of
Fut1 KO splenocytes on CD4 T cell proliferation and
differentiation, in comparison to WT splenocytes, and elucidated the
mechanisms involved. The comparative analysis of transcriptomes between
Fut1 KO and WT splenocytes revealed that thrombospondin (THBS)-1,
among the genes related to immune response and inflammation, was the
most highly downregulated gene in Fut1 KO splenocytes. The
reduced expression of THBS1 was further confirmed using qRT-PCR and flow
cytometry. In coculture experiments, Fut1 KO splenocytes promoted
the proliferation of CD4 T cells and drove their differentiation towards
Th1 and Th17 cells, compared to WT splenocytes. Moreover, the levels of
IL-2, IFN-γ and IL-17 were increased, while IL-10 was decreased, in T
cells cocultured with Fut1 KO splenocytes compared to those with
WT splenocytes. These effects of Fut1 KO splenocytes on T cells
were reversed when THBS1 was replenished. Taken together, our results
demonstrate that splenocytes with Fut1 deficiency promote CD4 T
cell proliferation and Th1/Th17 differentiation at least in part through
THBS1 downregulation.