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

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Science  15 Jan 1999:
Vol. 283, Issue 5400, pp. 390-392
DOI: 10.1126/science.283.5400.390

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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.

  • * These authors contributed equally to this work.

  • To whom correspondence should be addressed. E-mail: koyasu{at}sun.microb.med.keio.ac.jp

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