The development of unconventional T cells in the thymus depends on cognate interaction between invariant T cell receptors (TCRs) and antigen-presenting molecules. This interaction induces the expression of the transcription factor PLZF, which is essential for the differentiation of invariant natural killer T (iNKT) cells. However, the signaling cascade connecting surface invariant TCR to nuclear PLZF is not fully understood. We found that protein kinase D (PKD) is phosphorylated upon invariant TCR stimulation in iNKT cells. Mice lacking all PKD isoforms impaired PLZF induction and iNKT cell generation, which were rescued by introduction of a PLZF transgene. Using a phospho-proteomics approach, we identified Ikaros as a novel substrate for PKD in iNKT cells. Knock-in mice carrying a phosphorylation-defective mutant Ikaros displayed impaired iNKT cell development. Mechanistically, Ikaros binds to the upstream regulatory region of the PLZF gene, promoting its transcription in iNKT cells. These findings define a PKD-Ikaros axis that couples invariant TCR signaling to PLZF induction, thereby driving iNKT cell development.