Fig. 4: MAVS and STING signaling pathways maintain natural IELs in a TBK1-dependent but IFN-I-independent manner.
From: Dietary nucleic acids promote oral tolerance through innate sensing pathways in mice

a, b Quantification of the expression of Il15 at the mRNA level by qPCR (a) or protein level by ELISA (b) in the small intestine from WT, Tnfa−/−, or Tnfa−/−Tbk1−/−mice, n = 8. c–e Representative flow plots (c), cell percentages (d) and cell numbers (e) of small intestinal IELs from WT, Tnfa−/−, or Tnfa−/−Tbk1−/− mice, n = 5. f, g Quantification of the expression of Il15 at the mRNA level by qPCR (f) or protein level by ELISA (g) in the small intestine from WT, Ifnar1−/− or Ifnb1−/− mice, n = 8. h–j Representative flow plots (h), cell percentages (i) and cell numbers (j) of small intestinal IELs from WT, Ifnar1−/− or Ifnb1−/− mice, n = 6. k Quantification of the expression of IL-15 by ELISA in the small intestine from Ifnar1−/− mice fed ND or PD with or without supplement of 0.5% purified nucleic acids (NA), n = 6. Data are shown as mean ± s.e.m. and from one experiment representative of two (a, b, f, g, k) or three independent experiments (c–e, h–j). The P values were determined using one-way ANOVA followed by the Bonferroni post hoc test (a, b, d–g, i–k). Source data are provided as a Source Data file.