Autoimmunity in Autologous Islet Transplantation

Abstract

Total pancreatectomy (TP) is increasingly being utilized for definitive treatment in patients with debilitating chronic pancreatitis (CP). In an effort to prevent surgical diabetes, the procedure can be performed in conjunction with transplantation of islets of Langerhans recovered from the patients' own resected pancreas (autologous islet transplantation, AIT). Given that patients undergoing TP and AIT are traditionally assumed not to be at risk for the development of beta-cell autoimmunity, it is possible that the presence of autoimmune islet graft failure has been overlooked and underreported in this patient population. Herein, we describe two cases who underwent TP and AIT and later developed new-onset beta-cell autoimmunity (as evidenced by de novo glutamic acid decarboxylase antibody positivity), accompanied by complete insulin-dependent states. These cases emphasize the need for

Destructive inflammatory reaction after an autologous retinal pigment epithelium and choroid transplantation: no detection of an auto-immune response

“…The role of humoral autoimmunity in graft failure, activated by T-helper cells, has become more clear in recent years [14]. Presence of autoantibodies has been found after allogeneic and autologous transplantation [14][15][16][17]. Along the same line, we hypothesized that the inflammatory reaction was associated with an adaptive response of autoimmune origin resulting in the formation of detectable autoantibodies against RPE-choroid tissue and overrepresentation of a certain HLA type.…”

Islet Transplantation: How Much Have We Advanced and How to Keep Moving Forward?

“…The following articles in this theme introduce two somewhat unexplored issues with peri-and post-transplant care following total pancreatectomy and autologous islet transplantation (TPIAT): de novo onset of autoimmunity and the potential for portal hypertension. Ali et al [13] present two cases in which β-cell autoimmunity developed months following a TPIAT. In these cases, sudden deterioration of graft function was accompanied by elevated titers of typical β-cell autoantibodies (i.e., GAD, insulin, and islet cell), which were previously negative.…”