What question did this study set out to answer?

To understand how TNF signaling in myeloid cells mediates Th17 adjuvanticity of the CAF01 vaccine containing TDB.

Mincle-dependent Th17 adjuvanticity requires TNFR1 signaling in myeloid cells

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Conditional TNFR1 deficiency reveals myeloid cells as crucial for Th17 differentiation in vaccine response, implying TNF signaling's importance.

To understand how TNF signaling in myeloid cells mediates Th17 adjuvanticity of the CAF01 vaccine containing TDB.
Utilized conditional TNFR1-deficient mice to assess TNF signaling's role in myeloid cells, DC, and T cells.
Performed experiments with LysM-Cre, Clec9a-Cre, and CD11c-Cre deletion models.
Analyzed monocyte activation by TDB and cytokine production during Th17 induction.
LysM-Cre-mediated TNFR1 deletion in myeloid cells eliminated Th17 differentiation induced by the vaccine.
TNFR1 deletion in DC or T cells had minimal impact on Th17 induction.
Robust expression of Mincle and Th17-polarizing cytokines IL-1β and IL-6 was observed in activated monocytes, inhibited by Etanercept.

Blamberg et al. (2026) studied this question.

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Conditional TNFR1 deficiency reveals myeloid cells as crucial for Th17 differentiation in vaccine response, implying TNF signaling's importance.