Role of invariant natural killer T cells in lipopolysaccharide-induced pregnancy loss

• Wild-type and iNKT cell-deficient Jα18−/− mice were treated with LPS.
• iNKT cell deficient mice were less sensitive to LPS-induced embryo resorption.
• iNKT cells promote infection-associated decidual immune cell activation.
• iNKT cells augment inflammation-induced Th1-type cytokine secretion.
• iNKT cells are implicated in LPS-induced pregnancy loss.

We aimed to investigate the role of invariant natural killer T (iNKT) cells in infection-associated pregnancy loss. Wild-type (WT) C57BL/6 mice and iNKT cell-deficient Jα18−/− mice were treated with lipopolysaccharide (LPS). Embryo resorption rates (ERRs), decidual costimulatory molecule and activation molecule expression, and cytokine production were determined. WT and Jα18−/− mice were adoptively transferred with purified iNKT cells. ERRs, decidual costimulatory molecule and activation molecule expression, and cytokine production were assessed. LPS-treated Jα18−/− mice showed markedly reduced ERRs, decreased CD40, CD80, CD86, and CD69 expression, and reduced Th1 cytokine production at the maternal-fetal interface compared with WT mice. ERRs, expression of CD40, CD80, CD86, and CD69, and Th1 cytokine production in LPS-injected Jα18−/− mice following iNKT cell adoptive transfer were remarkably upregulated compared with control mice that did not receive adoptively transferred iNKT cells. Our results suggest that iNKT cells play an important role in LPS-induced pregnancy loss.