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A recessive defect in lymphocyte or granulocyte function caused by an integrated transgene
1Department of Immunology, Scripps Research Institute, La Jolla, California 92037.
The American Journal of Pathology
|November 1, 1992
Summary
Transgenic mice with a genetic defect show a severe lack of lymphocytes and abnormal granulocyte function. This leads to widespread tissue infiltration and organ enlargement, impacting immune cell regulation.
Area of Science:
- Immunology
- Genetics
- Transgenic animal models
Background:
- Insertional mutagenesis can disrupt gene function, leading to altered cellular processes.
- Transgenic mice are valuable models for studying genetic disorders and immune system regulation.
Purpose of the Study:
- To characterize a novel line of transgenic mice exhibiting immune system defects.
- To investigate the functional consequences of insertional mutagenesis on lymphocyte and granulocyte activity.
Main Methods:
- Generation and analysis of transgenic mice homozygous for a transgene integrant.
- Histopathological examination of tissues (lymph nodes, thymus, spleen, skin, liver, lung, kidney).
- Flow cytometry analysis of spleen lymphocyte populations.
Main Results:
- Homozygous transgenic mice displayed a near-complete absence of peripheral lymphocytes and a diminished thymus medulla.
- Enlarged spleens with a high percentage of blast cells were observed.
- Granulocyte and mononuclear infiltrates, immunoglobulin deposits, and arterial wall destruction occurred in multiple organs.
Conclusions:
- The identified genetic lesion specifically impacts lymphocyte and/or granulocyte activation regulation.
- This transgenic model offers insights into immune dysregulation and associated pathologies.
- Further research can elucidate the specific gene disrupted by the transgene.