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) 160 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 DAuthor
Demin Wang PhD Professor in the Microbiology and Immunology department at Medical College of WisconsinMESH 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
