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Function of CD4 molecules in LEC rat thymocytes
1Department of Parasitology and Immunology, University of Tokushima School of Medicine, Japan.
The Journal of Veterinary Medical Science
|November 1, 1996
Summary
The maturational arrest in Long-Evans Cinnamon (LEC) rat thymocytes is not caused by defects in CD4 or MHC class II molecules. This study found normal CD4 molecule function, ruling out these specific lymphocyte molecules as the cause.
Area of Science:
- Immunology
- Developmental Biology
- Genetics
Background:
- Long-Evans Cinnamon (LEC) rats exhibit an unexplained maturational arrest in thymocytes.
- Previous research ruled out Major Histocompatibility Complex (MHC) class II defects.
Purpose of the Study:
- To investigate the role of CD4 molecule function in the thymocyte maturational arrest observed in LEC rats.
Main Methods:
- Assessed the association of CD4 molecules with p56[lck] in LEC rat thymocytes.
- Measured intracellular calcium concentrations ([Ca2+]i) following anti-rat CD4 monoclonal antibody (mAb) cross-linking.
Main Results:
- CD4 molecules in LEC rat thymocytes normally associate with protein tyrosine kinase, p56[lck].
- Cross-linking CD4 molecules successfully triggered an increase in intracellular calcium concentrations ([Ca2+]i).
Conclusions:
- CD4 molecule function is normal in LEC rats.
- The thymocyte maturational blockade in LEC rats is not due to defects in CD4 or MHC class II molecules.