To investigate the interaction of B cells and Treg cells on a single-cell level.

Recent evidence suggests that an impaired peripheral B-cell tolerance accounts for elevated frequencies of pathogenic B cells in patients with multiple sclerosis (MS).  This effect might be conferred by a hampered control of T-cell dependent and/or T-cell independent B-cell activity through regulatory T cells (Treg). At present, little is known as to whether B cells are direct targets of Treg cells and how suppression of B-cell effector function is achieved. Possible mechanisms could be the modulation of immunoglobulin production, antigen presentation and cytokine secretion. Regulation of molecular calcium (Ca²⁺) influx is a key mechanism utilized by Treg cells to confer suppression in conventional CD4⁺ T cells (Tconv) as we could previously show.either Treg cells or Tconv.

Results: We found distinct patterns of Ca²⁺ signaling in CD27⁺ memory and CD27^- naïve B cells. We could further demonstrate that Ca²⁺ signals of B cells are reduced when co-cultured with Treg cells but not when co-cultured with Tconv.

We provide new information on Ca²⁺ signaling behaviour in B cells and B-cell subsets. We conclude that immediate inhibition of Ca²⁺ influx is likely to be a major mechanism of Treg cells to confer B-cell suppression.