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. 2020 Mar 7;69(7):1205–1216. doi: 10.1007/s00262-020-02535-6

Fig. 6.

Fig. 6

Adenosine affects the B cell receptor pathway. In B effector cells, binding of the antigen α-µ-F(ab’)2 to the BCR induces Syk and PIP3 activation supported by PI3K signaling. PIP3 recruits BTK, inducing auto-phosphorylation. The activated BTK activates PLCγ2 and IP3, binding to the endoplasmatic reticulum (ER), which secrets Ca2+. On Breg cells, extracellular ADO is produced by hydrolysis of ATP by the ectonucleotidases CD39 and CD73. ADO binds to different ADO receptors, downregulating the auto-phosphorylation of BTK and the Ca2+ influx in CD73neg B cells. In Breg cells, no BTK phosphorylation was found upon binding of the antigen α-µ-F(ab’)2