
STUDIES OF THE MECHANISM OF TOLERANCE INDUCED BY SHORT-TERM IMMUNOSUPPRESSION WITH CYCLOSPORINE IN HIGH-RISK CORNEAL ALLOGRAFT RECIPIENTS
Author(s) -
Eveline U. Irschick,
Katharine Miller,
Manuela Berger,
D Schönitzer,
Júlia Koller,
HeinzTheo Wagner,
W. Göttinger,
Carina Huber
Publication year - 1989
Publication title -
transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.45
H-Index - 204
eISSN - 1534-6080
pISSN - 0041-1337
DOI - 10.1097/00007890-198912000-00018
Subject(s) - ctl* , immunosuppression , transplantation , corneal transplantation , clone (java method) , immunology , cornea , medicine , clonal deletion , cytotoxic t cell , immune tolerance , biology , t cell , immune system , ophthalmology , in vitro , cd8 , t cell receptor , biochemistry , dna
Transplantation of unmatched allogeneic corneas into highly vascularized recipient eyes under the cover of short-term immunosuppression with cyclosporine enables permanent engraftment. The aim of this study was to further elucidate the mechanism(s) underlying this tolerant state. In eight "high-risk" cornea recipients the clone sizes of donor-specific and third-party reactive cytotoxic T cell precursors were assessed by limiting dilution analyses before and at three and six months after transplantation. Acquired allograft tolerance in these patients was not accompanied by clonal reduction of donor-specific CTL-p, whereas in the case of an irreversible rejection the donor-specific CTL pool size was significantly enlarged. This donor-specific CTL-p increase could already be seen two months before clinical manifestation. These patterns differed from that of tolerant renal transplant patients, in whom marked and donor-specific reduction of CTL-p was observed. During rejection identical patterns with increasing donor-specific CTL-p frequencies were seen in both groups of patients. We conclude that induction of tolerance by short-term CsA to unmatched cornea grafts is not caused by clonal reduction of the effector precursor cell pool.