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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 1.

Figure 1

MAdCAM-1 and HIV-1 gp120 bind to α4β7 in a cation dependent manner. (a) α4β7 expression detected by flow cytometry on freshly isolated primary B cells by an anti-β7 and anti-α4β7 (Act-1). (b) Variability of α4β7 expression on B cells from two separate donors. Flow cytometry shows that the binding of R66M gp120 (derived from a patient within the first month of infection) is proportional to β7 expression. β7 gating is based on an isotype control for each donor. (c) Binding of R66M gp120 to α4β7 on B cells. R66M gp120 binding to B cells in the presence of Ca2+/Mn2+ +/− anti-α4 (2B4), or in the absence of Ca2+/Mn2+ (EDTA buffer). MAdCAM-1 binding to B cells in the presence of Ca2+/Mn2+ +/− anti-α4 (2B4). Values reported indicate % of binding normalized to R66M (or MAdCAM-1) binding (100%), and are derived from 3 independent donors, p<0.0001 (one way ANOVA) (R66M n=3) (MAdCAM-1 n=2). (d) Comparison of the α4β7-reactivity of a panel of five recombinant gp120 preparations. α4β7-reactivity is reported as mean fluorescence intensity (MFI) of gp120s. An unlabeled anti-α4 (2B4) was included as a specificity control. Results are representative of at least three independent experiments using B cells from different donors.