Modulation of humoral islet autoimmunity by pancreas allotransplantation influences allograft outcome in patients with type 1 diabetes
Open accessAbstract
Pancreas transplantation in patients with type 1 diabetes presents allogeneic beta-cell autoantigens to the immune system long after the initial beta-cell destruction that leads to diabetes has occurred. The aims of this study were to determine whether re-exposure to beta-cell autoantigen through transplantation affect the humoral autoimmune response and whether its modulation correlates with graft outcome. Antibodies to the major autoantigens GAD (GADA) and protein tyrosine phosphatase IA-2 (IA-2A) were measured before and after transplantation in patients with type 1 diabetes who received pancreas and kidney allografts. In the 110 cases studied, pancreas graft survival was not significantly associated with the presence of GADA or IA-2A before transplantation. In the 75 patients with sequential follow-up samples up to 11.2 years after transplantation, autoantibodies were persistently undetectable in 44 cases (59%) and remained at stable detectable levels in 13 cases (17%). Substantial changes in antibody levels were found in 18 cases (24%), of which 13 cases (17%) had declining levels and 5 cases (7%) had marked increments after transplantation. Rising GADA and IA-2A levels in these five patients were predominantly of the IgG1 subclass, with progressive spreading of epitope reactivity. Pancreas graft function was lost 0.7-2.3 years after rising autoantibody levels in four of these five patients, and a significantly lower pancreas graft survival was found in patients with major rises in either GADA or IA-2A levels (P < 0.0001 vs. the remainder) and in patients having persistently high levels of IA-2A (P = 0.002 vs. stable antibody-negative patients). Kidney graft survival was not associated with islet autoantibody status. In conclusion, a minority of patients receiving pancreas allografts under generalized immunosuppression show a stimulation of islet autoantibody reactivity characteristic of that found in preclinical type 1 diabetes, which is almost invariably followed by graft function failure and resumption of insulin therapy.
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In islet cell or pancreas transplantation, the presence or absence of islet autoantibodies may indicate whether a subsequent failure of the transplanted islets is due to recurrent autoimmune disease or to rejection.
“In islet cell or pancreas transplantation, the presence or absence of islet autoantibodies may indicate whether a subsequent failure of the transplanted islets is due to recurrent autoimmune disease or to rejection (431).”
From Guidelines and Recommendations for Laboratory Analysis in the Diagnosis and Management of Diabetes Mellitus (2023) · cites this paper as [431]
The conclusion (RESEARCH DESIGN AND METHODS > B A; page unavailable) says that rising islet autoantibodies after pancreas transplantation may identify graft failures caused by recurrent autoimmunity. The paper does not establish that absent antibodies indicate rejection, and its own study concerns pancreas rather than islet-cell transplants. (LLM, conf=0.87)
Experimental — accuracy not yet measuredAfter islet or pancreas transplantation, islet cell autoantibody status may help distinguish recurrent autoimmune disease from rejection as the cause of graft failure.
“In islet cell or pancreas transplantation, the presence or absence of islet cell autoantibodies may clarify whether subsequent failure of the transplanted islets is due to recurrent autoimmune disease or to rejection (302).”
From Guidelines and recommendations for laboratory analysis in the diagnosis and management of diabetes mellitus (2011) · cites this paper as [302]
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References 8 · Cited by 90
- Authors
- Braghi, S., Bonifacio, E., Secchi, A., Di Carlo, V, Pozza, G., & Bosi, E.
- Affiliations
- Vita-Salute San Raffaele University (IT)
- Department of Medicine, Istituto Scientifico San Raffaele, San Raffaele Vita-Salute University, Milan, Italy.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2000-02-01
- Volume
- 49
- Issue
- 2
- Pages
- 218-224
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2124594387
- Cited by
- 90
- References
- 8
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 3 · 2022: 1 · 2021: 2 · 2020: 4 · 2019: 2 · 2018: 1 · 2016: 3 · 2015: 7 · 2014: 5 · 2013: 6 · 2012: 4
- FWCI
- 2.54
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Surgery › Transplantation: Methods and Outcomes
- Keywords
- pancreas transplantation, type 1 diabetes, islet autoimmunity, glutamic acid decarboxylase antibodies, IA-2 autoantibodies, beta cell autoantigens, allograft survival, graft failure, kidney transplantation, epitope spreading, IgG1 subclass, immunosuppression
- MeSH terms
- Adult, Antibody Formation, Epitopes, Autoantibodies, Autoantigens, Diabetes Mellitus, Type 1, Glutamate Decarboxylase, Graft Survival, Humans, Middle Aged, Postoperative Period, Transplantation, Homologous, Autoimmunity, Pancreas Transplantation, Treatment Outcome, Protein Tyrosine Phosphatases, Protein Tyrosine Phosphatase, Non-Receptor Type 1
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