Objective: To investigate the mechanism of GITRL on regulating the inflammatory reaction through the
programmed death ligand (PDL1) in Kupffer cells (KCs).
Methods: The KCs and the T cells were isolated and divided into 6 groups: (1) the Control group; (2) LPS group; (3)
LPS+Control siRNA group, transfected with Control siRNA; (4) LPS+GITRL siRNA group, transfected with GITRL
siRNA; (5) LPS+pEGFP-N1 control plasmid group, transfected with control plasmid; and (6) LPS+pEGFP-N1-GITRL
plasmid group, transfected with GITRL plasmid. The control group was co-cultured in DMEM only, whereas all of the
other groups were co-cultured with LPS (1 ug/m1). After 24 h of treatment, the expression levels of the TNF-α, GITRL,
and PDL1 in the supernatant, proliferation and apoptosis of T cells and the transposition of P65 in KCs were evaluated.
Results: The GITRL expression in KCs was obviously increased after LPS-stimulation in comparison to the control group.
Concurrently, PDL1 was inhibited, the T cells proliferated, and TNF-α levels in the supernatant were obviously increased in
the LPS group. With GITRL gene silencing, the restraint on PDL1 was clearly decreased, and the indexes of inflammation
were not as obvious as in the LPS group. Furthermore, the results of the pEGFP-N1-GITRL group were opposite from
that of the GITRL silencing group. However, the inflammation was exacerbated with the lower PDL1 expression.
Conclusions: Increasing the expression of GITRL in the KCs may promote the proliferation of T cells by restraining
PDL1, thus aggravating the inflammatory reaction. GITRL silencing could tilt the immunologic balance back and
restraining the inflammatory reaction.