Title:

Gli3 Regulates MHC II Expression in Dendritic Cell Subsets

Dendritic cells (DCs) are professional antigen-presenting cells that link innate and adaptive immune responses. The transcription factor Gli3, a component of the Hedgehog signaling pathway, is known to regulate tissue homeostasis and cellular differentiation. However, its role in dendritic cell function remains poorly understood. In this study, we utilized Gli3 conditional knockout mice to explore the impact of Gli3 deletion on the expression of major histocompatibility complex class II (MHC II) molecules in DC subsets. Flow cytometric analysis showed that the frequency of MHC II was 20% lower in conventional DC2 (cDC2) and monocyte-derived DCs (moDCs) derived from Gli3-deficient mice compared to wild-type controls. These findings suggest a potential role for Gli3 in regulating the antigen-presenting capacity of specific dendritic cell subsets and set the stage for further exploration into Gli3's role in immunoregulatory mechanisms.

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