Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 39, Issue 12, Pages 3395-3403Publisher
WILEY
DOI: 10.1002/eji.200939587
Keywords
B-cell Ag receptor; Cell cycle; ROS
Categories
Funding
- Cancer Research Institute
- NIH [GM37905, DE 16381]
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Superoxide and its derivatives have been implicated as secondary messenger molecules that influence signaling cascades in non-phagocytes. B lymphocytes produce superoxide after BCR ligation. We found that these ROS regulate B-cell signaling and entry into the cell cycle. B cells from mice deficient in the gp91(phox) subunit of the NADPH oxidase complex are unable to generate ROS after BCR ligation. However, after BCR stimulation, more gp91(phox) KO B cells enter the G1 stage of the cell cycle and proliferate than WT B cells. BCR ligation leads to a more rapid decrease in p27(Kip1) levels in gp91(phox) KO B cells. Gp91(phox) KO mice display enhanced T-cell-independent type 2, but normal T-dependent Ab responses. ROS-dependent regulation of BCR-induced proliferation may help modulate the size of the humoral response to T-cell-independent type 2 Ag immunization.
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