Defective development and function of Bcl10-deficient follicular, marginal zone and B1 B cells. Nat Immunol 2003 Sep;4(9):857-65
Date
08/12/2003Pubmed ID
12910267DOI
10.1038/ni963Scopus ID
2-s2.0-0041381357 (requires institutional sign-in at Scopus site) 164 CitationsAbstract
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.
Author List
Xue L, Morris SW, Orihuela C, Tuomanen E, Cui X, Wen R, Wang DMESH terms used to index this publication - Major topics in bold
Adaptor Proteins, Signal TransducingAnimals
Apoptosis
B-Cell CLL-Lymphoma 10 Protein
B-Lymphocyte Subsets
B-Lymphocytes
Bone Marrow
Carrier Proteins
Cell Division
Female
Flow Cytometry
Immunohistochemistry
In Situ Nick-End Labeling
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
NF-kappa B
Pneumococcal Infections
Streptococcus pneumoniae
