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IL-5 and Rp105 signaling defects in B cells from commonly used 129 mouse substrains.
1Immunology Division and Cancer and Haematology Division, The Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia. corcoran@wehi.edu.au
Journal of Immunology (Baltimore, Md. : 1950)
|November 26, 1999
Summary
The 129 mouse strain exhibits a defect in B lymphocyte responses to IL-5 and Rp105, impacting immune cell function. This genetic background influences mutant phenotypes and B-1 cell numbers.
Area of Science:
- Immunology
- Genetics
- Mouse Models
Background:
- The 129 mouse strain is widely used for generating genetically modified mice.
- The 129 genetic background can significantly influence the severity of mutant phenotypes.
- Understanding strain-specific effects is crucial for interpreting experimental results.
Purpose of the Study:
- To identify and characterize immune defects in commonly used 129 mouse substrains.
- To investigate the impact of the 129 genetic background on B lymphocyte responses.
- To determine the inheritance pattern of observed immune defects.
Main Methods:
- Analysis of B lymphocyte responses to Interleukin-5 (IL-5) and Rp105 stimulation.
- Assessment of B lymphocyte responses to surface Immunoglobulin M (IgM) stimulation.
- Evaluation of IL-5 receptor alpha-chain expression.
- Phenotypic analysis of peritoneal B-1 cell numbers.
Main Results:
- A specific defect in IL-5 and Rp105 responses was identified in two 129 mouse substrains.
- Surface IgM responses were diminished, though to a lesser extent.
- The defect significantly reduced IL-5 receptor alpha-chain expression.
- A codominant inheritance pattern was observed, with reduced peritoneal B-1 cell numbers in affected mice.
Conclusions:
- The 129 genetic background harbors a defect affecting B lymphocyte signaling pathways.
- This defect impacts IL-5 and Rp105 responses, potentially influencing immune cell function.
- Researchers using 129-derived mice should consider this genetic background's influence on immune phenotypes.