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Institut National de la Santé et de la Recherche Médicale, Unité 437, "Immunointervention dans les Allo et Xénotransplantations" and Institut de Transplantation et de Recherche en Transplantation, Centre Hospitalier Universitaire Hotel Dieu, Nantes, France;
Etablissement de Transfusion Sanguine, Nantes, France;
Harvard Medical School, Beth Israel, Deaconess Medical Center, Boston, MA 02215;
§
Service d’Anatomopathologie, Centre Hospitalier Universitaire Hotel Dieu, Nantes, France; and
¶
Service de Virologie, Institut de Biologie, Nantes, France
Chronic rejection represents a major cause of long-term kidney graft loss. T cells that are predominant in long-term rejected kidney allografts (35 ± 10% of area infiltrate) may thus be instrumental in this phenomenom, which is likely to be dependant on the indirect pathway of allorecognition only. We have analyzed the variations in T cell repertoire usage of the Vß chain at the complementary determining region 3 (CDR3) level in 18 human kidney grafts lost due to chronic rejection. We observed a strongly biased intragraft TCR Vß usage for the majority of Vß families and also a very high percentage (55%) of Vß families exhibiting common and oligoclonal Vß-Cß rearrangements in the grafts of patients with chronic rejection associated with superimposed histologically acute lesions. Furthermore, Vß8 and Vß23 families exhibited common and oligoclonal Vß-Jß rearrangements in 4 of 18 patients (22%). Several CDR3 amino acid sequences were found for the common and oligoclonal Vß8-Jß1.4 rearrangement. Quantitative PCR showed that biased Vß transcripts were also overexpressed in chronically rejected kidneys with superimposed acute lesions. In contrast, T lymphocytes infiltrating rejected allografts with chronic rejection only showed an unaltered Gaussian-type CDR3 length distribution. This pattern suggests that late graft failure associated with histological lesions restricted to Banff-defined chronic rejection does not involve T cell-mediated injury. Thus, our observation suggests that a limited number of determinants stimulates the recipient immune system in long-term allograft failure. The possibility of a local response against viral or parenchymatous cell-derived determinants is discussed.
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