Fanny Buron1, Sophie Reffet2, Lionel Badet3, Emmanuel Morelon1,4,5, Olivier Thaunat6,7,8,9. 1. Department of Transplantation, Nephrology and Clinical Immunology, Edouard Herriot Hospital, Hospices Civils de Lyon, 5 Place d'Arsonval, 69003, Lyon, France. 2. Department of Endocrinology and Diabetes, Lyon-Sud Hospital, Hospices Civils de Lyon, 69310, Pierre-Bénite, France. 3. Department of Urology and Transplantation surgery, Edouard Herriot Hospital, Hospices Civils de Lyon, Lyon, France. 4. French National Institute of Health and Medical Research (Inserm) Unit 1111, Lyon, France. 5. Lyon-Est Medical Faculty, Claude Bernard University (Lyon 1), Lyon, France. 6. Department of Transplantation, Nephrology and Clinical Immunology, Edouard Herriot Hospital, Hospices Civils de Lyon, 5 Place d'Arsonval, 69003, Lyon, France. olivier.thaunat@chu-lyon.fr. 7. French National Institute of Health and Medical Research (Inserm) Unit 1111, Lyon, France. olivier.thaunat@chu-lyon.fr. 8. Lyon-Est Medical Faculty, Claude Bernard University (Lyon 1), Lyon, France. olivier.thaunat@chu-lyon.fr. 9. Service de Transplantation, Néphrologie et Immunologie Clinique, Hôpital Edouard Herriot, 5 Place d'Arsonval, 69003, Lyon, France. olivier.thaunat@chu-lyon.fr.
Abstract
PURPOSE OF REVIEW: Grafted beta cells are lost because of recurrence of T1D and/or allograft rejection, two conditions diagnosed with pancreas graft biopsy, which is invasive and impossible in case of islet transplantation. This review synthetizes the current pathophysiological knowledge and discusses the interest of available immune biomarkers. RECENT FINDINGS: Despite the central role of auto-(recurrence of T1D) and allo-(T-cell mediated rejection) immune cellular responses, the latter are not directly monitored in routine. In striking contrast, there have been undisputable progresses in monitoring of auto and alloantibodies. Except for pancreas recipients in whom anti-donor HLA antibodies can be directly responsible for antibody-mediated rejection, autoantibodies (and alloantibodies in islet recipients) have no direct pathogenic effect. However, their fluctuation offers a surrogate marker for the activation status of T cells (because antibody generation depends on T cells). This illustrates the necessity to understand the pathophysiology when interpreting a biomarker and selecting the appropriate treatment.
PURPOSE OF REVIEW: Grafted beta cells are lost because of recurrence of T1D and/or allograft rejection, two conditions diagnosed with pancreas graft biopsy, which is invasive and impossible in case of islet transplantation. This review synthetizes the current pathophysiological knowledge and discusses the interest of available immune biomarkers. RECENT FINDINGS: Despite the central role of auto-(recurrence of T1D) and allo-(T-cell mediated rejection) immune cellular responses, the latter are not directly monitored in routine. In striking contrast, there have been undisputable progresses in monitoring of auto and alloantibodies. Except for pancreas recipients in whom anti-donor HLA antibodies can be directly responsible for antibody-mediated rejection, autoantibodies (and alloantibodies in islet recipients) have no direct pathogenic effect. However, their fluctuation offers a surrogate marker for the activation status of T cells (because antibody generation depends on T cells). This illustrates the necessity to understand the pathophysiology when interpreting a biomarker and selecting the appropriate treatment.
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