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. 2015 Jul 30;3(4):360–373. doi: 10.1002/iid3.74

Figure 2.

Figure 2

AR activation promotes bone marrow cells to differentiate into a novel DC subtype co‐expressing CD11c and Gr‐1. Mouse bone marrow cells cultured for 5 days in medium containing GM‐CSF (10 ng/mL) in the absence or presence of the indicated AR agonists/antagonist were stained with PE‐conjugated anti‐CD11b or anti‐CD11c antibodies and FITC‐conjugated anti‐Gr‐1 antibodies, then were examined by FACS analysis. A and B: Treatment of in vitro cultured BM cells with the A2BR agonist BAY 60‐6538 (100 nM), but not the A1R agonist CCPA (50 nM), the A2AR agonist CGS 21,680 (250 nM), or the A3R agonist 2‐Cl‐IB‐MECA (100 nM), promotes the differentiation of CD11c+Gr‐1+ BMDCs. C: The effect of the nonselective AR agonist NECA (100 nM) is blocked by the A2BR antagonist MRS 1754 (100 nM), but not the A1R antagonist DPCPX (50 nM), the A2AR antagonist SCH 58,261 (100 nM), or the A3R antagonist MRS1220 (5 µM). The results shown are from one representative experiment, which was repeated more than five times with similar results.