Type 1 diabetes results from an immune-mediated destruction of pancreatic beta cells. The disease can be transmitted by bone marrow transplantation in humans1 and animals.2,3 Furthermore, T cells that are reactive to several islet autoantigens have been identified in both mice and humans.4,5 Although it is generally accepted that T cells have a role during the disease process, the possible role of B cells and autoantibodies in type 1 diabetes in humans has not been fully resolved. When they are activated, B cells can produce autoantibodies to pancreatic beta-cell antigens — such as glutamic acid decarboxylase 65 (GAD65), . . .

https://www.nejm.org/doi/pdf/10.1056/NEJMoa010465

Development of type 1 diabetes despite severe hereditary B-cell deficiency.

Background
After the first investigational study on the use of extracorporeal photopheresis for the treatment of cutaneous T-cell lymphoma was published in 1983 with its subsequent recognition by the FDA for its refractory forms, the technology has shown significant promise in the treatment of other severe and refractory conditions in a multi-disciplinary setting. Among the major studied conditions are graft versus host disease after allogeneic bone marrow transplantation, systemic sclerosis, solid organ transplant rejection and inflammatory bowel disease.

Materials and methods
In order to provide recognized expert practical guidelines for the use of this technology for all indications the European Dermatology Forum (EDF) proceeded to address these questions in the hands of the recognized experts within and outside the field of dermatology. This was done using the recognized and approved guidelines of EDF for this task.

Results and conclusion
These guidelines provide at present the most comprehensive available expert recommendations for the use of extracorporeal photopheresis based on the available published literature and expert consensus opinion.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1111/jdv.12311

Guidelines on the use of extracorporeal photopheresis.

A cloned T-lymphocyte line, BDC-2.5, was derived from a nonobese diabetic (NOD) mouse and has been found to exhibit specificity for islet cell antigen in vitro and in vivo. This clone is a CD4+ T-lymphocyte that proliferates and makes lymphokine in response to islet cell antigen- and NOD antigen-presenting cells. In an in vivo transplantation system in which islet grafts were made in the presence or absence of the BDC-2.5 T-lymphocytes, it was found that incorporation of the islet-specific T-lymphocytes into the graft site resulted in complete destruction of the transplanted tissue. Similar grafts made with pituitary tissue were not affected by the T-lymphocyte clone. These results suggest that the islet-specific T-lymphocytes mediate islet destruction in a tissue-specific manner.

T-lymphocyte clone specific for pancreatic islet antigen.

Cytoplasmic islet cell autoantibodies (ICAs) of 13 coded sera were determined by 26 laboratories. ICAs were determined by 24 laboratories according to a standard protocol based on the conventional indirect-immunofluorescence technique on cryostat sections of human pancreas. In addition, these 24 laboratories had performed any of 8 modifications of the assay. Test samples were titrated to end point, and the results obtained with the different methods were compared with those obtained by the standard protocol. The remaining 2 laboratories used either exclusively pancreatic sections of monkey instead of human as substrate (lab 23) or applied immunohistochemical staining (lab 22). By following the standard protocol, interlaboratory concordance was greater than 90% for the presence or absence of islet cell antibodies in 7 of the 13 samples circulated. However, a wide variability of titers was recorded, ranging from negative to 128. Of the modifications, prolonged incubation in the presence of aprotinin was performed by 10 laboratories and was found to improve the sensitivity in 57 of 70 (81%) determinations with samples that had been ICA positive by the standard protocol. Improved sensitivity was also noted by 2 laboratories with sections of monkey pancreas. Acetone-fixed sections, used by 6 laboratories, or a two-color immunofluorescence method, applied by 3 laboratories, did not change the titers in 27 of 35 (77%) and 14 of 25 (56%) determinations with samples that had been ICA positive by the standard protocol. In contrast, heat inactivation of the samples before testing, performed by 5 laboratories, resulted in a decrease in titers in 25 of 39 (64%) determinations.(ABSTRACT TRUNCATED AT 250 WORDS)

Progress Toward Standardization of Cytoplasmic Islet Cell–Antibody Assay

Supernatants of peripheral blood mononuclear cells from healthy human donors stimulated with recall antigen (purified protein derivative of tuberculin) or lectin (phytohaemagglutinin) markedly inhibited the insulin release from isolated human and rat islets of Langerhans, and decreased rat islet contents of insulin and glucagon in a dose-dependent manner. A maximal effect on islet function was obtained with supernatant concentrations down to 5%. Supernatants of mononuclear cells stimulated with tuberculin were more potent than supernatants produced by lectin stimulation. Culture medium reconstituted with tuberculin or phytohaemagglutinin did not impair islet function. Electron microscopy demonstrated that supernatants were cytotoxic to islet cells. The cytotoxic mononuclear cell mediator(s) was non-dialysable, sensitive to heating to 56 degrees C, labile even when stored at -70 degrees C, but stable when lyophilised.

Mechanisms of pancreatic islet cell destruction. Dose-dependent cytotoxic effect of soluble blood mononuclear cell mediators on isolated islets of Langerhans.

Disappearance and reappearance of islet cell cytoplasmic antibodies in cyclosporin-treated insulin-dependent diabetics.

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Disappearance and reappearance of islet cell cytoplasmic antibodies in cyclosporin-treated insulin-dependent diabetics.