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Receptor editing in CD45-deficient immature B cells
Shoham Shivtiel1, Nira Leider, Doron Melamed
1Department of Immunology, Bruce Rappaport Faculty of Medicine and Rappaport Family Institute for Research in the Medical Sciences, Technion-Israel Institute of Technology, Haifa, Israel.
European Journal of Immunology
|September 5, 2002
Summary
CD45 deficiency does not prevent B cell receptor editing in mice encountering self-antigens. Immature B cells lacking CD45 still undergo receptor editing, a key B cell tolerance mechanism.
Area of Science:
- Immunology
- Cellular Biology
- Molecular Biology
Background:
- B cell receptor (BCR) signaling threshold is crucial for eliminating self-reactive B cells.
- Receptor editing is a primary mechanism of B cell tolerance, involving secondary light chain recombination.
- CD45, a protein tyrosine phosphatase, positively regulates BCR signaling.
Purpose of the Study:
- To investigate the role of BCR signaling competence in inducing tolerance-mediated receptor editing.
- To determine if CD45 deficiency affects receptor editing in autoreactive B cells.
Main Methods:
- Utilized 3-83 transgenic (Tg) mice expressing B cell receptors specific for MHC class I antigen K(k).
- Crossed 3-83 Tg mice with CD45-deficient mice (CD45-/-).
- Employed an IL-7-driven bone marrow (BM) culture system to study B cell development and receptor editing.
Main Results:
- In 3-83 Tg CD45(-/-) mice, allelic exclusion was efficiently imposed, though peripheral B cell numbers were reduced.
- Immature 3-83 Tg CD45(-/-) B cells encountering self-antigen showed developmental arrest.
- These arrested cells underwent secondary light chain recombination and receptor editing, similar to CD45-sufficient cells.
Conclusions:
- The absence of CD45 does not eliminate the capacity for receptor editing in immature B cells.
- Immature B cells lacking CD45 retain competence for receptor editing when encountering high-avidity membrane-bound self-antigens.