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Exaggerated and persistent cutaneous delayed-type hypersensitivity in transgenic mice whose epidermal keratinocytes
A Nasir1, B Ferbel, W Salminen
1Department of Dermatology, University of Rochester School of Medicine and Dentistry, New York 14642.
The Journal of Clinical Investigation
|August 1, 1994
Summary
Transgenic mice engineered to express B7-1 in skin keratinocytes showed heightened immune responses. This suggests keratinocytes play a key role in regulating skin inflammation by dampening T cell activation.
Area of Science:
- Immunology
- Dermatology
- Genetics
Background:
- Mouse keratinocytes act as tolerogenic antigen-presenting cells (APCs) influencing T cell activation.
- The role of keratinocyte-expressed co-stimulatory molecules in immune regulation is not fully understood.
Purpose of the Study:
- To investigate the in vivo function of B7-1 expression in epidermal keratinocytes.
- To determine the impact of targeted B7-1 expression on T cell-mediated immune responses in the skin.
Main Methods:
- Generation of transgenic mice with keratin 14 promoter-driven B7-1 expression in epidermal keratinocytes.
- Assessment of B7-1 cell surface protein expression using CTLA-4/Ig fusion protein.
- Evaluation of immune responses through epicutaneous challenge with haptens (e.g., fluorescein isothiocyanate).
Main Results:
- Transgenic mice exhibited high levels of B7-1 on epidermal keratinocytes.
- Skin histology and immune cell populations (Langerhans cells, dendritic epidermal T cells) remained normal.
- Transgenic mice displayed enhanced and prolonged delayed-type hypersensitivity responses compared to controls.
Conclusions:
- Epidermal keratinocyte-presented B7-1 can modulate T cell responses, leading to amplified skin inflammation.
- Tolerogenic antigen presentation by keratinocytes normally dampens T cell-mediated inflammation in the skin.
- Dysregulation of B7-1 expression in epidermal cells may contribute to chronic skin disorders characterized by hyperresponsiveness.
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