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Spontaneous skin ulceration and defective T cell function in CD18 null mice
K Scharffetter-Kochanek1, H Lu, K Norman
1Department of Molecular and Human Genetics, Houston, Texas 77030, USA.
The Journal of Experimental Medicine
|July 7, 1998
Summary
Mice lacking CD18, a key component of leukocyte integrins, developed severe dermatitis and impaired T cell responses. This CD18 null mouse model is crucial for understanding integrin function in vivo.
Area of Science:
- Immunology
- Cell Biology
- Genetics
Background:
- Leukocyte integrins, such as CD11/CD18, are critical for immune cell function.
- CD18 is the common beta2 subunit shared by several leukocyte integrins.
Purpose of the Study:
- To investigate the in vivo function of CD18 by creating and analyzing a CD18 null mouse model.
- To elucidate the role of CD18 in neutrophil trafficking and T cell responses.
Main Methods:
- Generation of CD18 null mice via gene targeting.
- Phenotypic analysis including clinical signs, cell counts, and immunoglobulin levels.
- Intravital microscopy to assess neutrophil adhesion.
- Assessment of T cell proliferation upon stimulation with specific antigens.
Main Results:
- CD18 null mice exhibited chronic dermatitis with facial erosions and elevated neutrophils, immunoglobulins, and plasma cells.
- Neutrophil recruitment to inflamed skin and adhesion to venules were severely impaired.
- T cell proliferation was significantly defective in response to staphylococcal enterotoxin A and alloantigens.
Conclusions:
- CD18 is essential for proper neutrophil function and trafficking in vivo.
- CD11/CD18 integrins play a more significant role in T cell responses than previously recognized.
- The CD18 null mouse is a valuable tool for studying integrin-mediated immune processes.