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Impaired B Cell Development and Proliferation in Absence of Phosphoinositide 3-Kinase p85α

Fruman, David A., Snapper, Scott B., Yballe, Claudine M., Davidson, Laurie, Yu, Jonathan Y., Alt, Frederick W., Cantley, Lewis C.·1999·Science
DOI 10.1126/science.283.5400.393
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Abstract

Phosphoinositide 3-kinase (PI3K) activation has been implicated in many cellular responses, including fibroblast growth, transformation, survival, and chemotaxis. Although PI3K is activated by several agents that stimulate T and B cells, the role of PI3K in lymphocyte function is not clear. The mouse gene encoding the PI3K adapter subunit p85α and its splice variants p55α and p50α was disrupted. Most p85α-p55α-p50α −/− mice die within days after birth. Lymphocyte development and function was studied with the use of the RAG2-deficient blastocyst complementation system. Chimeric mice had reduced numbers of peripheral mature B cells and decreased serum immunoglobulin. The B cells that developed had diminished proliferative responses to antibody to immunoglobulin M, antibody to CD40, and lipopolysaccharide stimulation and decreased survival after incubation with interleukin-4. In contrast, T cell development and proliferation was normal. This phenotype is similar to defects observed in mice lacking the tyrosine kinase Btk.

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Metadata

Authors
Fruman, D. A., Snapper, S. B., Yballe, C. M., Davidson, L., Yu, J. Y., Alt, F. W., & Cantley, L. C.
Affiliations
D. A. Fruman. C. M. Yballe, J. Y. Yu, L. C. Cantley, Division of Signal Transduction, Beth Israel Deaconess Medical Center, Boston, MA 02215, and Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA. S. B. Snapper, Department of Medicine, Harvard Medical School, Boston, MA 02115; Howard Hughes Medical Institute, Children's Hospital, Boston, MA 02115; Center for Blood Research, Boston, MA 02115; and Gastrointestinal Unit (Medical Services), Massachusetts General Hospital, Boston,...
Venue
Science
Publisher
American Association for the Advancement of Science (AAAS)
Published
1999-01-15
Volume
283
Issue
5400
Pages
393-397
ISSN
  • 0036-8075
  • 1095-9203
DOI
10.1126/science.283.5400.393
Cited by
516
References
0
Language
en

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