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. Author manuscript; available in PMC: 2021 Jan 16.
Published in final edited form as: Mol Cell. 2019 Dec 2;77(2):384–394.e4. doi: 10.1016/j.molcel.2019.10.031

Figure 2: HMCES leads to a B cell intrinsic defect in CSR.

Figure 2:

A) Representative flow cytometry plots showing CSR to IgG1 and IgA in B cells isolated from Hmces+/+ and Hmces−/− mice and stimulated with anti-CD40, IL-4, TGF-β and IL-5 for 5 days. B) Bar graphs quantifying the kinetics of IgM to IgA switching in primary B cells from Hmces+/+ and Hmces−/− mice. C) Bar graphs quantifying the kinetics of IgM to IgG1 switching in primary B cells isolated from Hmces+/+ and Hmces−/− mice stimulated with anti-CD40, IL-4, TGF-β and IL-5. D) Bar graphs quantifying the kinetics of IgM to IgG1 switching in primary B cells isolated from Hmces+/+ and Hmces−/− mice and stimulated with anti-CD40 and IL-4. E) Bar graphs quantifying the kinetics of IgM to IgE switching in primary B cells isolated from Hmces+/+ and Hmces−/− mice and stimulated with anti-CD40 and IL-4. F) Bar graphs quantifying the kinetics of IgM to IgG3 switching in primary B cells isolated from Hmces+/+ and Hmces−/− mice and stimulated with LPS. Data are represented as mean ± SD. Each dot represents cells isolated from an individual mouse and lines are used to highlight samples analyzed in the same experiment. Statistical significance was calculated using two-way ANOVA. *p value ≤0.005, **p value ≤0.001.