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Background/Aims:Human invariant natural killer T(iNKT) cells express a TCR Vα 24-Jα Q paired with Vβ 11 and are activated by a surrogate ligand,α-galactosylceramide(α GalCer) .The iNKT cells are involved in the regulation of anti-viral immune responses;however,little is known about their roles in hepatitis C virus(HCV) infection.Methods:We compared the frequency of peripheral iNKT cells and their cytokine producing capacity reactive to α GalCer between chronically HCV-infected patients and healthy subjects.Cytokine production of freshly isolated iNKT cells were analyzed by ELISPOT.Activated iNKT cells were obtained by culture with α GalCer-loaded dendritic cells(DCs) and re-stimulated with them for the measurement of cytokine production.Results:The frequencies of iNKT cells were not different between HCV-infected patients and healthy subjects.The number of fresh IFN-γ-producing iNKT cells reactive to α GalCer was not different between the patients and controls,whereas fresh iNKT cells produced negligible amounts of Th2 cytokines regardless of HCV infection.In response to α GalCer,expanded iNKT cells from the patients secreted IFN-γ comparable in amount to controls,whereas they released significantly more IL-13 than cells from controls.Conclusions:Activated iNKT cells from HCV-infected patients gain more ability to secrete IL-13 than those from healthy subjects.
Background / Aims: Human invariant natural killer T (iNKT) cells express a TCR Vα 24-Jα Q paired with Vβ 11 and are activated by a surrogate ligand, α-galactosylceramide (α GalCer). The iNKT cells are involved in the regulation of anti-viral immune responses; however, little is known about their roles in hepatitis C virus (HCV) infection. Methods: We compared the frequency of peripheral iNKT cells and their cytokine producing capacity reactive to α GalCer between chronically HCV-infected patients and healthy Subjects. Cytokine production of freshly isolated iNKT cells were analyzed by ELISPOT. Activated iNKT cells were obtained by culture with α GalCer-loaded dendritic cells (DCs) and re-stimulated with them for the measurement of cytokine production. Results: The frequencies of iNKT cells were not different between HCV-infected patients and healthy subjects. The number of fresh IFN-γ-producing iNKT cells reactive to α GalCer was not different between the patients and controls, but fresh iN KT cells produced negligible amounts of Th2 cytokines regardless of HCV infection. In response to α GalCer, expanded iNKT cells from the patients secreted IFN-γ comparable in amount to controls, there they they released significantly more IL-13 than cells from controls. Conclusions: Activated iNKT cells from HCV-infected patients gain more ability to secrete IL-13 than those from healthy subjects.