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B cell abnormality and autoimmune disorders.
1Laboratory of Immunology, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan. tsubata.imm@mri.tmd.ac.jp
Autoimmunity
|October 22, 2005
Summary
Defects in B cell apoptosis, a key process for removing self-reactive cells, are common in lupus models. This impaired B cell apoptosis may contribute to systemic autoimmune diseases like lupus by failing to eliminate harmful self-reactive B cells.
Area of Science:
- Immunology
- Autoimmunity
- Cell Biology
Background:
- Patients with systemic autoimmune diseases, including systemic lupus erythematosus (SLE), exhibit various B cell abnormalities.
- While many B cell abnormalities are not clearly linked to disease pathogenesis, a defect in B cell apoptosis is consistently observed in lupus-prone animal models.
Purpose of the Study:
- To investigate the role of B cell antigen receptor (BCR)-mediated apoptosis in the pathogenesis of systemic autoimmune diseases.
- To determine if defects in BCR-mediated apoptosis contribute to the failure in deleting self-reactive B cells in lupus.
Main Methods:
- Analysis of B cell apoptosis in various lupus-prone mouse models, including spontaneous (NZB x NZW)F1, MRL/lpr, and genetically engineered models (Bim-deficient, CD40L-transgenic).
- Examination of B cell antigen receptor (BCR) ligation-induced apoptosis in mature B cells.
Main Results:
- A defect in mature B cell apoptosis induced by BCR ligation is a common finding across multiple lupus-prone mouse models.
- This impaired apoptosis suggests a failure in the normal deletion of self-reactive B cells.
Conclusions:
- Defects in BCR-mediated apoptosis represent a widely observed B cell abnormality in lupus-prone mice.
- Abrogation of self-reactive B cell deletion due to impaired BCR-mediated apoptosis may play a significant role in the pathogenesis of systemic autoimmune diseases like lupus.