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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Defective development and function of Bcl10-deficient follicular, marginal zone and B1 B cells.

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.[1]

References

  1. Defective development and function of Bcl10-deficient follicular, marginal zone and B1 B cells. Xue, L., Morris, S.W., Orihuela, C., Tuomanen, E., Cui, X., Wen, R., Wang, D. Nat. Immunol. (2003) [Pubmed]
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