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. Author manuscript; available in PMC: 2024 May 1.
Published in final edited form as: Allergy. 2022 Dec 7;78(5):1204–1217. doi: 10.1111/all.15595

Figure 6: FcεRIβ and MS4A6A exhibit redundancy in IgE-dependent human mast cell degranulation.

Figure 6:

(A) Dose-responsive degranulation of LAD2 cells stimulated with streptavidin following treatment with standard control oligonucleotide (black), FcεRIβ SSO (blue), MS4A6A SSO (green), and combined FcεRIβ + MS4A6A SSOs; (B) LAD2 cells treated with SSOs degranulate in response to stimulation with Compound 48/80 through an IgE-independent mechanism; (C) Dose-responsive degranulation of HLMCs stimulated with α-IgE following treatment with standard control oligonucleotide (black), FcεRIβ SSO (blue), MS4A6A SSO (green), and combined FcεRIβ + MS4A6A SSOs; (D) HLMC cells treated with SSOs degranulate in response to stimulation with thapsigargin through an IgE-independent mechanism. (E) Western blot analysis of MS4A6A and FcεRIα expression with and without IL-4 treatment for 7 days. Β-actin was used as a loading control. (F) Dose-responsive degranulation of CBMCs stimulated with α-IgE following treatment with standard control oligonucleotide (black), FcεRIβ SSO (blue), MS4A6A SSO (green), and combined FcεRIβ + MS4A6A SSOs (red). Data are the mean±SEM from at least three independent experiments. *P < 0.05, **P < 0.01, ANOVA with post-test.