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. 2008 Dec 22;205(13):3091–3103. doi: 10.1084/jem.20081163

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© 2008 Murn et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 4. — The suppressive effect of PGE2 on B cell proliferation is mediated by the EP4 receptor. Ptger4^+/+ (A) and Ptger4^−/− (B) splenic B cells were incubated in vitro for 60 h with anti-IgM F(ab′)₂ and cotreated with PGE2 at the concentrations as indicated (ctrl, vehicle-treated control). Bar, 200 μm. (C) BCR-stimulated splenic B cells were cotreated as indicated for 60 h, followed by determination of ATP content. Final concentrations of PGE1-OH and AH-13205 were adjusted to compensate for the differences between inhibitory constants for the mouse EP4 receptor (56). RLU, relative luminescence units. Error bars are the SD of triplicates. (D) The CFSE staining method was used to follow proliferation of Ptger4^+/+ and Ptger4^−/− mouse B cells. Flow cytometry analysis of viable cells is shown (see Materials and methods).