Expression of TASK‐2 and its upregulation by B cell receptor stimulation in WEHI‐231 mouse immature B cells

Abstract

Stimulation of B cell receptors (BCR‐ligation) induces apoptosis of immature B cells, which is critical to the elimination of self‐reactive clones. In the mouse immature B cell line WEHI‐231, we previously reported two types of background K+ channels with large‐ (~ 300 pS, LKbg) and medium (~ 100 pS, MKbg) conductance in divalent cation‐free conditions. LKbg has been recently identified as TREK‐2, however, the molecular nature of MKbg is not known yet. In the present study, we found that the background K+ conductance of WEHI‐231 was markedly increased by BCR‐ligation. A single channel study revealed that MKbg activity was increased by BCR‐ligation, and that the biophysical properties of MKbg were consistent with those of TASK‐2. The expression of TASK‐2 and its upregulation by BCR‐ligation was confirmed by RT‐PCR and immunoblot assays in WEHI‐231. The BCR‐ligation‐induced increase of K+ current was prevented by calcineurin inhibitors (cyclosporine A or FK506), and also by TASK‐2 specific siRNA transfection (si‐TASK‐2). Furthermore, si‐TASK‐2 attenuated the apoptosis of WEHI‐231 caused by BCR‐ligation. TASK‐2 activity and its mRNA were also confirmed in the primary splenic B cells of mouse. Summarizing, the authors report for the first time the expression of TASK‐2 in B cells, and surmise that the upregulation of TASK‐2 by BCR‐ligation is associated with the apoptosis of immature B cells.