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Invariant natural killer T (iNKT) cells are a major subset of NKT cells that recognize foreign and endogenous lipidantigens presented by CD1d. Although iNKT cells are characteristically autoreactive to self-antigens, the role ofiNKT cells in the regulation of cytotoxic T lymphocytes (CTL) has been elucidated using α-galactosylceramide(α-GalCer), a strong synthetic glycolipid that is presented by professional antigen presenting cells (APCs), such asdendritic cells. Despite the well-known effects of α-GalCer and dendritic cells on lipid antigen presentation, thephysiological role of endogenous antigens presented by CTLs during crosstalk with iNKT cells has not yet beenaddressed. In this study, we found that antigen-primed CTLs with transient CD1d upregulation could present lipid selfantigensto activate the iNKT cell production of IFN-γ. CTL-mediated iNKT cell activation in turn enhanced IFN-γproduction and the proliferation and cytotoxicity of CTLs. We also found that the direct interaction of iNKT cells andCTLs enhanced the antitumor immune responses of CTLs. This partially explains the functional role of iNKT cells in CTLmediatedantitumor immunity. Our findings suggest that in the absence of exogenous iNKT cell ligands, iNKT cellsenhanced the CTL production of IFN-γ and CTL proliferation and cytotoxicity via direct interaction with CD1dexpressed on T cells without interacting with APCs.
