Abstract
A central problem in improving the success of renal transplantation in humans is to discover how to induce in the recipient an active immunological unresponsiveness to the donor's alloantigens1–3. There is increasing evidence that immunological unresponsiveness can be induced by either suppressor T cells4,5 or antibodies directed against the T-cell receptor, that is, anti-idiotypic antibodies6,7. In our institutes, there are now six successful renal recipients. One of these, CD-S5, is a 32 year old man, HLA tissue-typed as Aw31, Bw39, Bw54 and DRw4. He received a second kidney transplant from a cadaveric donor having HLA-A2 and B5 on 21 August, 1975, after the first transplant from his brother with Aw26 and Bw40 had been rejected. The stimulation index of the mixed lymphocyte reaction (MLR) between patient and first donor was 11.9 but MLR could not be tested in the second grafting. One year after the second graft, immunosuppressive treatment with azathioprine was withdrawn because of drug toxic hepatitis. In spite of the administration of only prednisolone at 10 mg per day for the past 3yr, the patient's creatinine clearance has remained at 70 ml min−1. We proposed that the long survival of the renal graft might be due to an immunological unresponsiveness induced by the host immunoregulatory mechanism of this patient. To test this possibility, we have investigated the patient's serum for factor(s) capable of suppressing the host immune response. We report here our finding that the patient's serum contained an antibody against a T-cell receptor for a certain MLR, which was capable of specifically inhibiting a certain MLR.
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Miyajima, T., Higuchi, R., Kashiwabara, H. et al. Anti-idiotypic antibodies in a patient with a functioning renal graft. Nature 283, 306–308 (1980). https://doi.org/10.1038/283306a0
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DOI: https://doi.org/10.1038/283306a0
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