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. Author manuscript; available in PMC: 2017 Mar 5.
Published in final edited form as: Nat Immunol. 2016 Sep 5;17(11):1273–1281. doi: 10.1038/ni.3552

Figure 3.

Figure 3

MUC1-ST engagement of Siglec-9 during the differentiation of monocytes into inflammatory macrophages results in the generation of dysfunctional cells. (a) Flow cytometry histograms showing CD86 expression by LPS & IFNγ differentiated M-CSF macrophages after treatment with MUC1-ST on day 0 in the presence of isotype control or anti-Siglec-9 or anti-IL-6Rα and (b) bar graphs summarizing the data from multiple independent donors. (c) IL-12 p70 release from macrophages treated as in (a,b). (d,e,f) Day 0 MUC1-ST treated M-CSF macrophages were co-cultured with autologous CD8+ or CD4+ T cells in the presence of anti-CD3 and anti-CD28 beads and proliferation (d) or expression of CD69 (e) were measured by flow cytometric analysis. (f) Density plots showing % of CD69+CD25+ CD8+ T cells co-cultured with autologous M-CSF macrophages treated with MUC1-ST and antibody (isotype, anti-Siglec-9 or anti -L-6Rα). N=3 independent donors (b,c,d,e); Representative data from 3 independent donors showing similar results (f). Data shown are the mean and s.e.m. P = *<0.05, **<0.01, as determined by Student’s paired t-test (b,c,d,e).