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. Author manuscript; available in PMC: 2014 Jun 1.
Published in final edited form as: Nat Immunol. 2013 Oct 27;14(12):1256–1265. doi: 10.1038/ni.2746

Figure 2.

Figure 2

An α4β7-reactive gp120 inhibits α-IgM + CpG induced B cell proliferation. (a) CFSE proliferation assay of α-IgM + CpG induced proliferation of B cells in the presence of gp120s. An α4β7-reactive gp120 (R66M) blocks proliferation, while a gp120 with minimal affinity for α4β7 (92Th14.12) fails to block proliferation. B cells were cultured with B cell stimuli (α-IgM + CpG) with or without gp120s for 96 h. (b) Division Index (FlowJo) indicating the average number of cell divisions in cells from the original population from 5 independent donors. Treatment stimuli denoted below the x-axis, p<0.001 (two-way ANOVA) (n=5). (c) A dose response utilizing three increasing concentrations of a gp120 with a high affinity for α4β7 (R880F) were employed. (d) Light scatter overlay of freshly isolated (red), α-IgM + CpG stimulated (blue), and α-IgM + CpG + gp120 stimulated (green) B cells. (e) Flow-cytometry based cell cycle analysis of α-IgM + CpG stimulated (blue), and α-IgM + CpG + gp120-stimulated (green) B cells stained with PI (x-axis). Data reported are representative of three independent experiments.

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