Impaired B cell development and proliferation in absence of phosphoinositide 3-kinase p85α Academic Article Article uri icon


MeSH Major

  • Fatty Acids
  • Neoplasms


  • 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 p85alpha and its splice variants p55alpha and p50alpha was disrupted. Most p85alpha-p55alpha-p50alpha-/- 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.

publication date

  • January 15, 1999



  • Academic Article


Digital Object Identifier (DOI)

  • 10.1126/science.283.5400.393

PubMed ID

  • 9888855

Additional Document Info

start page

  • 393

end page

  • 7


  • 283


  • 5400