| First Author | Xue L | Year | 2003 |
| Journal | Nat Immunol | Volume | 4 |
| Issue | 9 | Pages | 857-65 |
| PubMed ID | 12910267 | Mgi Jnum | J:85147 |
| Mgi Id | MGI:2672996 | Doi | 10.1038/ni963 |
| Citation | Xue L, et al. (2003) Defective development and function of Bcl10-deficient follicular, marginal zone and B1 B cells. Nat Immunol 4(9):857-65 |
| abstractText | Bcl10 is an intracellular protein essential for nuclear factor (NF)-kappaB 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-kappaB efficiently after stimulation with lipopolysaccharide. Bcl10-deficient marginal zone B cells did not capture antigens, and Bcl10-deficient (Bcl10-/-) 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. |
