Xid-Like Immunodeficiency in Mice with Disruption of the p85α Subunit of Phosphoinositide 3-Kinase
H Suzuki, Y Terauchi, M Fujiwara, S Aizawa, Y Yazaki… - Science, 1999 - science.org
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−/− or xid (X-linked immunodeficiency) mice. These results provide evidence that p85α
is functionally linked to the Btk pathway in antigen receptor–mediated signal transduction …
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−/− or xid (X-linked immunodeficiency) mice. These results provide evidence that p85α
is functionally linked to the Btk pathway in antigen receptor–mediated signal transduction …
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.
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