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Langerhans' cell depletion by staphylococcal superantigens
S Pickard1, G Shankar, K Burnham
1Department of Microbiology and Molecular Genetics, Oklahoma State University, Stillwater 74078.
Immunology
|December 1, 1994
Summary
Certain staphylococcal enterotoxins deplete Langerhans' cells (LC) in mouse skin. This LC depletion involves GTP-binding proteins and protein synthesis, similar to ultraviolet radiation effects.
Area of Science:
- Immunology
- Dermatology
- Microbiology
Background:
- Langerhans' cells (LC) are critical immune cells in the epidermis.
- Superantigens, like staphylococcal enterotoxins, can modulate immune responses.
- Previous research linked ultraviolet radiation to LC depletion.
Purpose of the Study:
- To investigate the impact of staphylococcal enterotoxins on Langerhans' cell distribution in mouse skin.
- To elucidate the molecular mechanisms underlying superantigen-induced LC depletion.
Main Methods:
- Cultured mouse skin sections were treated with specific staphylococcal enterotoxins.
- Expression of LC markers (ATPase and IA) was analyzed.
- Inhibitors of GTP-binding proteins, kinases, protein, and RNA synthesis were used.
Main Results:
- Staphylococcal enterotoxin A and exfoliative toxin, but not toxic shock syndrome toxin, significantly depleted LC.
- LC depletion was blocked by cholera toxin, pertussis toxin, and H-8, indicating involvement of GTP-binding proteins.
- Inhibition of protein or RNA synthesis also prevented LC depletion.
Conclusions:
- Staphylococcal enterotoxins can induce Langerhans' cell depletion in mouse skin.
- The signaling pathway involves GTP-binding proteins and protein synthesis.
- These mechanisms mirror those observed for ultraviolet radiation-induced LC depletion.