Twenty-one patients with fixed drug eruption were studied with the lymphocyte transformation test. In no patient was there blast transformation when the responsible drug (1:10,000 dilution) was added to the lymphocyte culture. The addition to the lymphocyte culture of 0.4 ml of autologous serum, taken at the acme of the clinical reaction, produced blast transformation of the lymphocytes, and when the responsible drug (1:10,000 dilution) was added to this system, blast transformation increased by several times. The addition of the responsible drug to autologous serum obtained during clinical remission produced a minimal or negative response. These findings suggest that during fixed drug eruptions a blast transforming factor appears temporarily in the serum and increases its activity in the presence of the responsible drug. This factor spontaneously diminishes or disappears a few days after clinical exacerbation.
Twenty-five patients with clinically proven, patch test positive nickel dermatitis were studied with the lymphocyte transformation test (LTT). Serial dilutions of NiS04 were present in the lymphocyte culture. None of the controls showed lymphocyte blast transformation. In fourteen patients maximal incorporation of thymidine occurred at the highest dilutions (i :5O,ooo-i :ioo,ooo). In eleven patients the highest incorporation occurred at the lower dilutions. The nature of the antigen responsible for the specific reaction remains unknown.Allergic contact dermatitis due to nickel hypersensitivity has commonly been studied by the patch test method using an aqueous solution of nickel sulphate. Several workers have used the lymphocyte transformation test (LTT) in patch test positive nickel sensitive subjects (a more sensitive technique for the detection of contact hypersensitivity.In an attempt to find a better understanding of some of the reported results, we have investigated the effect of using various doses of nickel sulphate in the LTT. This nickel salt is one for which there are no published reports of non-specific stimulation of lymphocytes. MATERIALS AND METHODSTwenty-five patients with clinically confirmed nickel contact dermatitis were studied. All patients were patch tested on the skin of the upper back with a 2-5% (o-i6 mol/1) aqueous solution of nickel sulphate (NiS04, 7H2O), (Merck), 0-25 ml (0-3 mmol), spread on an area of i cm^ and read after 48 h. On removal of the patch all patients showed a vesicular reaction which persisted for several days. LTT was performed on each patient using serial dilutions of nickel sulphate. Ten normal people without a history of eczema and with a negative patch test to NiS04 were used as controls.
The cutaneous lymphocyte-associated antigen defines T lymphocytes with cutaneous tropism under inflammatory conditions. Bacterial infections participate in cutaneous inflammations, such as atopic dermatitis or psoriasis. Bacterial superantigens, such as staphylococcal enterotoxin B, can activate peripheral blood mononuclear cells to induce effector T cells bearing the T cell skin homing receptor cutaneous lymphocyte-associated antigen via enhancement of interleukin-12 production. We have identified and characterized the anti-inflammatory effects of different phosphodiesterase inhibitors on this system. Our data indicate that the selective type 4 phosphodiesterase inhibitor rolipram inhibits the Staphylococcal enterotoxin B-mediated generation of cutaneous lymphocyte-associated antigen positive CD3+ cells from peripheral blood mononuclear cells by reducing interleukin-12 production in a concentration-dependent manner. Conversely, type 3 phosphodiesterase or type 5 phosphodiesterase selective inhibitors were not effective. The rolipram inhibitory effect was on interleukin-12 production, as exogenously added interleukin-12 could revert rolipram suppression. These results suggest that selective type 4 phosphodiesterase inhibition may have beneficial effects on T cell mediated skin inflammatory processes characterized by the presence of bacterial infections, that are thought to exacerbate ongoing skin inflammation.
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