Abstract
Normal C3WHeN strain mice exposed to topical 8inethoxypsomlen plus long wave ultraviolet (PUVA) showed a reduction in contact hypersensitivity, (CH) which was localized to the skin in the area of PUVA treatment (local suppression), whereas systemic PUVA treatment caused diffuse suppression of CH reaction, regardless of the application site of 2,4-dinitro-1-fluorobenzene (DNFB).
There seem to be two different mechanisms responsible for CH reduction by PUVA. Local suppression by topical PUVA treatment was thought to be a result of blocking the afferent phase of immune response, it was associated with a lack of CH effector cells in the peripheral lymph nodes and could not be reversed by indomethacin treatment. Diffuse suppression induced by systemic PUVA treatment seemed to be associated with blocking of egress of effector cells from the regional lymph nodes, this depressed CH response was prevented when indomethacin was administered before PUVA treatment.