期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 22, 期 24, 页码 8580-8591出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.22.24.8580-8591.2002
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资金
- NCI NIH HHS [P30 CA021765, CA21765] Funding Source: Medline
- NHLBI NIH HHS [P01 HL053749, HL53749] Funding Source: Medline
- NIDDK NIH HHS [R01 DK42932, R01 DK042932] Funding Source: Medline
Many receptor and nonreceptor tyrosine kinases activate phosphoinositide 3-kinases (PI3Ks). To assess the role of the delta isoform of the p110 catalytic subunit of PI3Ks, we derived enzyme-deficient mice. The mice are viable but have decreased numbers of mature B cells, a block in pro-B-cell differentiation, and a B1 B-cell deficiency. Both immunoglobulin M receptor-induced Ca2+ flux and proliferation in response to B-cell mitogens are attenuated. Immunoglobulin levels are decreased substantially. The ability to respond to T-cell-independent antigens is markedly reduced, and the ability to respond to T-cell-dependent antigens is completely eliminated. Germinal center formation in the spleen in response to antigen stimulation is disrupted. These results define a nonredundant signaling pathway(s) utilizing the delta isoform of p110 PI3K for the development and function of B cells.
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