This PDF file includes:

• Fig. S1. Normal T cell and B cell development in Lck-GLK Tg mice.
• Fig. S2. Inflammatory phenotypes and enhanced T_H17 differentiation in Lck-GLK Tg mice.
• Fig. S3. Autoimmune responses in Lck-GLK Tg mice are abolished by IL-17A deficiency.
• Fig. S4. GLK transgene does not regulate IL-23 receptor expression, STAT3 phosphorylation, and RORγt-binding element at the −120 region of the IL-17A promoter.
• Fig. S5. PKCθ controls Ser³⁶ phosphorylation–mediated AhR nuclear translocation and AhR-mediated autoimmune responses.
• Fig. S6. PKCθ directly interacts with AhR in the cytoplasm of Lck-GLK T cells.
• Fig. S7. Autoimmune responses in Lck-GLK Tg mice are reduced by PKCθ KO.
• Fig. S8. TCR signaling induces in vivo interaction between AhR and RORγt.
• Fig. S9. Schematic model of AhR/RORγt-mediated IL-17A transcription in T cells of Lck-GLK Tg mice with different gene-KO backgrounds.
• Table S1. Transcription factors of NF-κB–mediated cytokines.
• References (58, 59)

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