Elucidation of the Inhibitory Immune Mechanism of the Contact Hypersensitivity in Mice Induced by Ultraviolet Irradiation.
- Author:
Jum Yul CHOI
;
Hyung Sun SOHN
;
Seok Don PARK
;
Hun Taeg CHUNG
- Publication Type:Original Article
- Keywords:
Ultraviolet irradiation;
Contact hypersensitivity;
Langerhans cell;
Prostaglandin;
Indomethacin
- MeSH:
Animals;
Dermatitis, Contact*;
Indomethacin;
Langerhans Cells;
Lymph Nodes;
Mice*;
Plasma;
Prostaglandins E;
Skin
- From:Korean Journal of Dermatology
1987;25(5):573-576
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Normal C3H/HeN strain mice exposed to low-dose ultraviolet radiation(4 * 400 J/m) demonstrated a reduction in contact sensitization potential which locaiized to the skin area of direct UVR exposure(local suppression), where high-dose exposure of UVR(1*30.000 J/m) caused systemic suppression of CH induction, regardless of the application site of 2,4-dinitro-l-fluorobenzene(DNFB). There seemed to be two different mechanisms that are responsible for CH reaction induced by UVR. One of them, local suppression of low-dose UVR resulted from blocking the afferent phase of immune response by the functiona] inactivation of the epidermal Langerhans cells ; it was associated with lack of CH effector cells in the peripheral lymph nodes, an enhanced splenic suppressor cell acitvity, and could not be reversed by indomethacin treatment. The other, systemic suppression of high-dose UVR was mediated by enhancement of prostaglandin E(PGE); it was associated with prevention of the egress of effector cells within the regional lymph node which was caused by blocking the efferent lymphatics, and elevated plasma level of PGE. And depressed CH response was reversed when treated by indomethacin.
