Abstract
Bcl10 is an intracellular protein essential for nuclear factor (NF)-κB activation after lymphocyte antigen receptor stimulation. Using knockout mice, we show that absence of Bcl10 impeded conversion from transitional type 2 to mature follicular B cells and caused substantial decreases in marginal zone and B1 B cells. Bcl10-deficient B cells showed no excessive apoptosis. However, both Bcl10-deficient follicular and marginal zone B cells failed to proliferate normally, although Bcl10-deficient marginal zone B cells uniquely failed to activate NF-κB efficiently after stimulation with lipopolysaccharide. Bcl10-deficient marginal zone B cells did not capture antigens, and Bcl10-deficient (Bcl10-l-) mice failed to initiate humoral responses, leading to an inability to clear blood-borne bacteria. Thus, Bcl10 is essential for the development of all mature B cell subsets.
Original language | English (US) |
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Pages (from-to) | 857-865 |
Number of pages | 9 |
Journal | Nature Immunology |
Volume | 4 |
Issue number | 9 |
DOIs | |
State | Published - Sep 1 2003 |
Externally published | Yes |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology