The early activation of memory B cells from Wiskott-Aldrich syndrome patients is suppressed by CD19 downregulation.

ABSTRACT: Wiskott-Aldrich syndrome (WAS) pediatric patients exhibit a deficiency in humoral immune memory. However, the mechanism by which Wiskott-Aldrich syndrome protein (WASP) regulates the differentiation and activation of memory B cells remains elusive. Here we examine the early activation events of memory B cells from the peripheral blood mononuclear cells of WAS patients and age-matched healthy controls (HCs) using total internal reflection fluorescence microscopy. In response to stimulation through the B-cell receptor (BCR), memory B cells from HCs showed significantly higher magnitudes of BCR clustering and cell spreading than naive B cells from the same individuals. This was associated with increases in CD19 recruitment to the BCR and the activation of its downstream signaling molecule Btk

SUBMITTER: Bai X 

PROVIDER: S-EPMC5043127 | biostudies-literature | 2016 Sep

REPOSITORIES: biostudies-literature