Degranulating dermal mast cells in UV-B-irradiated skin have been implicate
d for many years in the mechanisms of irradiation erythema. There is now co
nsiderable evidence that dermal mast cells are important to the processes b
y which both UV-B radiation and cis-urocanic acid (cis-UCA) suppress immune
responses to sensitizing antigens applied to non-irradiated/non-cis-UCA-ex
posed sites. Mast-cell-depleted mice are resistant to the immunosuppressive
effects of UV-B radiation and cis-UCA for 'systemic' immunomodulation. How
ever, these mice gain responsiveness if the dorsal skin is reconstituted si
x weeks prior to irradiation or cis-UCA administration at that site with cu
ltured bone-marrow-derived mast cells from + / + mice. The molecular trigge
rs for initiating mast-cell degranulation are being actively sought. Eviden
ce suggests that histamine, and not tumour necrosis factor a, is the major
mast-cell product that signals altered immune responses to sensitizing anti
gens applied to non-irradiated, non-cis-UCA-exposed sites. Histamine may ha
ve multiple roles, but experiments with indomethacin administered to mice h
ave shown that one process involves induction of prostanoid production. (C)
2000 Elsevier Science S.A. All rights reserved.