This study investigates the role of Janus kinase 1 (JAK1) signaling within dendritic cells (DCs) in maintaining peripheral immune tolerance. Using a mouse model with DC-specific deletion of JAK1, researchers observed exacerbated experimental autoimmune encephalomyelitis (EAE), characterized by increased CD4+ T cell proliferation and reduced regulatory T cell (Treg) induction. The findings highlight the importance of JAK1-STAT1 signaling in DCs for upregulating PD-L1 expression, which is crucial for the conversion of naive CD4+ T cells into Tregs and the suppression of autoimmune responses.
JAK1 signaling in DCs is essential for PD-L1 expression and the induction of Tregs, thereby promoting peripheral tolerance and mitigating autoimmune pathology in EAE.
DC-specific JAK1 Knockout mouse model, generated by crossing Jak1^flox/flox mice with CD11c-Cre transgenic mice to achieve targeted deletion of JAK1 in dendritic cells.
Autoimmunity, Peripheral tolerance, Dendritic cells, Regulatory T cells, PD-L1, JAK-STAT signaling
Conditional Knockout model, CD11c-Cre, Jak1^flox/flox, Dendritic cell-specific gene deletion
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