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Mast cells in UV-B-induced immunosuppression
P H Hart1, M A Grimbaldeston, J J Finlay-Jones
1Department of Microbiology and Infectious Diseases, School of Medicine, Flinders University, Adelaide, Australia. Prue.Hart@flinders.edu.au
Journal of Photochemistry and Photobiology. B, Biology
|August 15, 2000
Summary
UV-B radiation and cis-urocanic acid (cis-UCA) suppress immune responses by degranulating dermal mast cells. Histamine, released by mast cells, signals these altered immune responses, potentially through prostanoid production.
Area of Science:
- Immunology
- Dermatology
- Photobiology
Background:
- Dermal mast cells are implicated in UV-B-induced erythema.
- Mast cells play a crucial role in UV-B radiation and cis-urocanic acid (cis-UCA) mediated immunosuppression.
- Mast-cell-depleted mice exhibit resistance to UV-B and cis-UCA immunosuppressive effects.
Purpose of the Study:
- To investigate the role of dermal mast cells in UV-B and cis-UCA-induced immunosuppression.
- To identify the key mast cell mediators responsible for altered immune responses.
- To elucidate the signaling pathways involved in mast cell-mediated immunosuppression.
Main Methods:
- Utilizing mast-cell-depleted mice models.
- Reconstitution of dorsal skin with bone-marrow-derived mast cells.
- Administration of UV-B radiation and cis-UCA.
- Treatment with indomethacin to investigate prostanoid production.
Main Results:
- Mast-cell-depleted mice are resistant to UV-B and cis-UCA immunosuppression.
- Reconstitution with mast cells restores UV-B and cis-UCA sensitivity.
- Histamine, not TNF-alpha, appears to be the primary mast cell mediator signaling altered immune responses.
- Histamine's action involves the induction of prostanoid production.
Conclusions:
- Dermal mast cells are essential for UV-B and cis-UCA-induced immunosuppression.
- Histamine is a key mediator released by mast cells, influencing immune responses to sensitizing antigens.
- Prostanoid production is a significant downstream effect of histamine signaling in this context.