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. 2022 Jan 4;19(2):260–275. doi: 10.1038/s41423-021-00812-7

Fig. 8. The therapeutic effect of systemic sFLT3L requires Batf3-dependent cDC1s and can be mediated by iNKT cells.

Fig. 8

Batf3KO (a), Rag1KO (d, e), and WT mice (b, c, f) were fed an HFD for 7  weeks. At week 4, the mice were treated with a hydrodynamic (HD) injection of a plasmid expressing sFlt3L (mflex) or an empty vector, as shown in Fig. 7a. a Body weight gain of Batf3KO mice (empty vector n = 7; mflex n = 9). Quantification of Treg (b) and NKT cells (c) present in the WAT of WT mice treated with mflex or the empty vector. d Body weight gain of RagKO mice (d, n = 9 in both groups). e Body weight gain of RagKO mice with or without adoptive transfer of iNKT cells (n = 6 mflex; n = 9 Empty vector + iNKT cells; n = 9 mflex + iNKT cells). f Body weight gain of WT mice treated with or without an anti-NK1.1 depleting antibody (n = 9 mflex; n = 10 mflex + anti-NK1.1). (a, b, c, d, f) Significance was assessed by an unpaired two-tailed Student’s t-test. e Significance was assessed by one-way ANOVA with Sidak’s correction for multiple comparisons *P < 0.05, **P < 0.01; ***P < 0.001. Each point represents a biological replicate. a, d, e, f Data are shown as the mean ± SEM, and the same mice were measured repeatedly