Runt-related Transcriptional Factor3Is Involved In The Change Of Phenotype And Function In ThPok-deficient Invariant Natural Killer T-cells

The interplay between the CD4-lineage transcription factor ThPok and the CD8-lineage transcription factor Runx3(runt-related transcription factor3) in T-cell development is extensively documented, however, little is understood about their roles in invariant natural killer T (iNKT) cells. Since it is known that CD Id-restricted iNKT cells are committed to the CD4+CD8-and CD4-CD8-sublineages that respond to antigen stimulation with rapid and potent release of the T helper (Th) cytokines such as Thl and Th2type cytokines, and previous reports have demonstrated a new population of CD8+NKT cells in ThPok-deficient mice, we set out to determine whether Runx3is involved in the re-expression of CD8and the function of iNKT cells in the absence of ThPok. In this study, we used mice lacking Runx3,ThPok, or both to verify that Runx3was partially responsible for the appearance of CD8+iNKT cells in ThPok knockout mice, and further, in the absence of ThPok, Runx3participated in the immune response of iNKT cells in acute hepatitis induced by a-galactosylceramide. Thus, these results revealed that Runx3is crucial for the phenotypic and functional changes in iNKT cells from ThPok-deficient mouse.