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Genetic defect in responsiveness to the B cell mitogen lipopolysaccharide
European Journal of Immunology
|May 1, 1977
Summary
Splenic B cells in C57BL/10ScCr mice lack lipopolysaccharide (LPS) response and receptor. However, their B cells maintain responses to purified protein derivative and lipoprotein.
Area of Science:
- Immunology
- Cell Biology
Background:
- Splenic B cells from C57BL/10ScCr mice exhibit an unresponsiveness to lipopolysaccharide (LPS).
- These B cells do not express a known "LPS receptor" identified serologically.
Purpose of the Study:
- To investigate the specific B cell response defect in C57BL/10ScCr mice regarding lipopolysaccharide (LPS).
- To determine if other polyclonal B cell activation pathways are functional in these mice.
Main Methods:
- Analysis of splenic B cell activation.
- Use of lipopolysaccharide (LPS) as a mitogen.
- Assessment of responses to purified protein derivative and lipoprotein.
Main Results:
- Splenic B cells from C57BL/10ScCr mice demonstrated a failure to respond to the mitogenic effects of lipopolysaccharide (LPS).
- Absence of a serologically defined "LPS receptor" was confirmed on these B cells.
- Polyclonal B cell activation by purified protein derivative of tuberculin and lipoprotein remained intact.
Conclusions:
- The C57BL/10ScCr mouse model presents a specific defect in lipopolysaccharide (LPS) B cell signaling.
- This defect does not broadly impair B cell function, as responses to other stimuli are preserved.