Two-faced protein both inhibits and activates B cell receptor signaling

Researchers have found that restoration of B cell function in BCR signaling deficiencies involves the interaction of CD22, normally an inhibitory factor, with binding partners on the same cell, which results in upregulation of BCR expression and paradoxically increased BCR signaling. These findings suggest that CD22 could be a novel target for the treatment of patients with B cell signaling deficiencies such as X-linked agammaglobulinemia.