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Defective development and function of Bcl10-deficient follicular, marginal zone and B1 B cells. Nat Immunol 2003 Sep;4(9):857-65

Date

08/12/2003

Pubmed ID

12910267

DOI

10.1038/ni963

Scopus ID

2-s2.0-0041381357   150 Citations

Abstract

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 D

Author

Demin Wang PhD Assistant Professor in the Microbiology and Immunology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Adaptor Proteins, Signal Transducing
Animals
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
jenkins-FCD Prod-398 336d56a365602aa89dcc112f077233607d6a5abc