Summary The systemic effect of ultraviolet (UV) irradiation on delayed type hypersensitivity (DTH), contact hypersensitivity (CHS) and allograft rejection was investigated in BALB/c mice which had been exposed to a single 1 h treatment with UV radiation (27 kJ/m^) from FS40 sunlamps (60% UVB). After UV irradiation (3-5 days), mice were treated on an unirradiated site with either a subcutaneous injection of allogeneic spleen cells or a topical application of the contact scnsitizer oxazolone (OX). The DTH response to allogeneic cells and the CHS response to OX elicited 6 days afterimmunization were significantly lower in UV-treated mice than in normal mice. Spleen cells from these animals were transferred intravenously into X-irradiated (600R) recipients which were immediately challenged with antigen and the DTH or CHS response elicited was determined 24 h later. Recipients of equal numbers ofcells from sensitized and normal animals (6X10^ from each donor) exhibited positive DTH or CHS responses to the antigen used to sensitize the donor. In contrast, recipients of equal numbers ofcells from animals sensitized and UV suppressed to the same antigen showed a suppressed DTH or CHS response. This suppression was antigen-specific. Treatment ofcells from UV suppressed animals, prior to transf^er, with complement and cytotoxic anti-Lyt 2 or anti-Thy 12 monoclonal antibodies abrogated the suppressive ability of these cells, in contrast to cytotoxic treatment with anti-L3T4 or anti-Lyt 1 monoclonal antibodies which had no significant effeet. The suppressor cells therefore had the phenotype Thy 12 + , Lyt 2 + , L3T4"'. Lyt l^. In a separate series of experiments BALB/c miee, either untreated or given I h of U V irradiation 3-5 days previously, were given a heart or skin allograft from a C3H/He donor. The primarily vascularized cardiac ailografts survived significantly longer in UV-irradiated than in normal recipients (median survival time 13 daysvs 10 days, /'=0 035), but the survival of C3H/He skin ailografts was unaltered in UV mice. No identification of suppressor populations was carried out in the heart allograft recipients. These experiments provide the basis for investigations ofthe possible role of UV-induced antigen-specific suppressor cells in modulating responses to alloantigens.

In the murine cardiac model for vascularised transplantation graft function may be monitored by direct palpation, electrocardiography, and graft histology. To assess the merits of these methods, and to measure ischaemic damage, isografts and allografts were examined at regular intervals from 0 to 60 days after grafting. Heart transplants were vascularised from the abdominal great vessels, using microsurgical techniques, with ischaemic times of less than 60 min. Isografts showed no decrease in heart rate over 60 days, as measured by palpation and electrocardiography, but the voltage of the ventricular complex fell progressively over the first 28 days after grafting then remained stable for more than 60 days. The voltage drop was associated with atrophy of myocardial tissue. Allografts in recipients treated with rabbit antimouse antilymphocyte serum were maintained for more than 60 days with little change in palpation rate or recorded heart rate but with significant falls in ventricular complex voltage, reflecting myocardial atrophy and fibrosis. Untreated allografts were rejected in 10-14 days and showed a rapid fall in palpated heart rate, measured heart rate, and ventricular complex voltage. Thus, in this study, palpation of the heart graft gave an accurate measure of the pulse rate and correlated with electrical activity in acutely rejecting grafts, but in long surviving grafts measurement of ventricular complex voltage showed myocardial damage that was not detectable by direct palpation.

The effect of Cyclosporine A (CsA) on T cell-mediated delayed-type hypersensitivity (DTH) reactions to murine alloantigens was analysed by transferring spleen cells from sensitised and suppressed mice into irradiated naive recipients. Selective removal of Thy1+, Ly1+ or Ly2+ cells prior to intravenous transfer of cells from alloantigen-sensitised mice showed that Ly1+ Thy1+ cells transferred sensitivity. Concomitant treatment of mice with alloantigen and CsA suppressed the DTH response to alloantigens, and spleen cells transferred from these suppressed mice abrogated the response of sensitised cells transferred at the same time. The suppressor cells were strain-restricted and antigen-specific with the surface phenotype Thy + , Ly1–– Ly2+.

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