Figure 4.
Depletion of BM B cells during Abx treatment is independent of type I and II IFN signaling. (A) Pathway enrichment analysis of the B-cell lineage cluster from single cells combined from BM from WT mice treated for 14 days with the vehicle Ctrl or Abx cocktail in drinking water reveals upregulated and downregulated enriched pathways in Ctrl mice compared with Abx-treated mice. (B) Enrichment plots show that IFN-γ and IFN-α responses were among the pathways most enriched in BM B cells from Ctrl mice, as compared with Abx-treated mice. (C) Multiplex-based quantification of relevant serum cytokines IFN-1B, ISG, IP-10, and IFN-γ in mice exposed to 4 weeks of Abx or Ctrl conditions in 1 representative experiment. (D) BM populations of B-cell progenitors were quantified in mice lacking type I (Ifnar1−/−), type II (Ifngr1−/−), and type I and II (Ifnar1−/−Ifngr1−/−) IFN signaling, and Stat1 (Stat1−/−)-deficient mice compared with WT mice. For panel C, the Mann-Whitney U test was used to test statistical significance between the groups; and for panel D, the Kruskal-Wallis test was used. Data are displayed as mean ± SEM from 2 independent experiments. ∗P ≤ .05; ∗∗P ≤ .01. IFN-1B, type I IFN IFN-β1; IP-10, IFN-γ–induced protein 10; ISG, IFN-stimulated gene.

Depletion of BM B cells during Abx treatment is independent of type I and II IFN signaling. (A) Pathway enrichment analysis of the B-cell lineage cluster from single cells combined from BM from WT mice treated for 14 days with the vehicle Ctrl or Abx cocktail in drinking water reveals upregulated and downregulated enriched pathways in Ctrl mice compared with Abx-treated mice. (B) Enrichment plots show that IFN-γ and IFN-α responses were among the pathways most enriched in BM B cells from Ctrl mice, as compared with Abx-treated mice. (C) Multiplex-based quantification of relevant serum cytokines IFN-1B, ISG, IP-10, and IFN-γ in mice exposed to 4 weeks of Abx or Ctrl conditions in 1 representative experiment. (D) BM populations of B-cell progenitors were quantified in mice lacking type I (Ifnar1−/−), type II (Ifngr1−/−), and type I and II (Ifnar1−/−Ifngr1−/−) IFN signaling, and Stat1 (Stat1−/−)-deficient mice compared with WT mice. For panel C, the Mann-Whitney U test was used to test statistical significance between the groups; and for panel D, the Kruskal-Wallis test was used. Data are displayed as mean ± SEM from 2 independent experiments. ∗P ≤ .05; ∗∗P ≤ .01. IFN-1B, type I IFN IFN-β1; IP-10, IFN-γ–induced protein 10; ISG, IFN-stimulated gene.

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