Monitoring inflammation, humoral and cell-mediated immunity in pancreas and islet transplants

Paolo Monti, Debora Vignali, Lorenzo Piemonti

Research output: Contribution to journalArticlepeer-review


Type 1 diabetes (T1D) is caused by the chronic autoimmune destruction of insulin producing beta cells. Beta cell replacement therapy through whole pancreas or islet transplantation is a therapeutic option for patients in which a stable glucose control is not achievable with exogenous insulin therapy. Long-term insulin independence is, however, hampered by the recipient immune response that includes activation of inflammatory pathways and specific allo- and autoimmunity. The identification and monitoring of soluble and cellular biomarkers are of critical relevance for the prediction of graft damage, for the evaluation of responses to immune-modulating therapy, and for target pathways identification to generate novel drugs or therapeutic approaches. The final objective of immune monitoring is to find ways to improve the outcome of pancreas and islet transplantation. In this review, we discuss the available tools to monitor the innate, humoral and cellular responses after islet and pancreas transplantation, and the most relevant findings generated by these measurements.

Original languageEnglish
Pages (from-to)135-143
Number of pages9
JournalCurrent Diabetes Reviews
Issue number3
Publication statusPublished - Jun 1 2015


  • Autoantibodies
  • Autoreactive T cells
  • Diabetes
  • Homeostatic proliferation
  • Immune monitoring
  • Islet transplantation
  • Pancreas transplantation

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology


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