Xid -Like Immunodeficiency in Mice with Disruption of the p85α Subunit of Phosphoinositide 3-Kinase

Abstract

Mice with a targeted gene disruption of p85α, a regulatory subunit of phosphoinositide 3-kinase, had impaired B cell development at the pro–B cell stage, reduced numbers of mature B cells and peritoneal CD5⁺ Ly-1 B cells, reduced B cell proliferative responses, and no T cell–independent antibody production. These phenotypes are nearly identical to those of Btk^−/− orxid (X-linked immunodeficiency) mice. These results provide evidence that p85α is functionally linked to the Btk pathway in antigen receptor–mediated signal transduction and is pivotal in B cell development and functions.