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

Liquan Xue; Stephan W. Morris; Carlos Orihuela; Elaine Tuomanen; Xiaoli Cui; Renren Wen; Demin Wang

doi:10.1038/ni963

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

Liquan Xue, Stephan W. Morris, Carlos Orihuela, Elaine Tuomanen, Xiaoli Cui, Renren Wen, Demin Wang

Research output: Contribution to journal › Article › peer-review

158 Scopus citations

Abstract

Bcl10 is an intracellular protein essential for nuclear factor (NF)-κB 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-κB efficiently after stimulation with lipopolysaccharide. Bcl10-deficient marginal zone B cells did not capture antigens, and Bcl10-deficient (Bcl10^-l-) 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.

Original language	English (US)
Pages (from-to)	857-865
Number of pages	9
Journal	Nature Immunology
Volume	4
Issue number	9
DOIs	https://doi.org/10.1038/ni963
State	Published - Sep 1 2003
Externally published	Yes

ASJC Scopus subject areas

Immunology and Allergy
Immunology

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abstract = "Bcl10 is an intracellular protein essential for nuclear factor (NF)-κB 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-κB efficiently after stimulation with lipopolysaccharide. Bcl10-deficient marginal zone B cells did not capture antigens, and Bcl10-deficient (Bcl10-l-) 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.",

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AU - Xue, Liquan

AU - Morris, Stephan W.

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AU - Tuomanen, Elaine

AU - Cui, Xiaoli

AU - Wen, Renren

AU - Wang, Demin

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AB - Bcl10 is an intracellular protein essential for nuclear factor (NF)-κB 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-κB efficiently after stimulation with lipopolysaccharide. Bcl10-deficient marginal zone B cells did not capture antigens, and Bcl10-deficient (Bcl10-l-) 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.

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

Abstract

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