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.

Cyclosporine-induced renal dysfunction in experimental animals and humans

Ten patients with rheumatoid arthritis were entered into a 24-week pilot study of oral cyclosporin A at a starting dosage of 6 mg/kg/day, followed by a 12-week washout period. Significant improvement in clinical parameters was observed at 12 weeks and 24 weeks (P less than 0.02 versus baseline for joint pain and joint swelling indexes and patient and physician assessments; P less than 0.04 versus baseline in the numbers of painful/tender joints and swollen joints). Adverse reactions were varied: renal impairment occurred in all patients and hypertension occurred in 7. All patients demonstrated an increase in defined disease activity at cessation of treatment and through the washout period. Cyclosporin A is clinically effective in the treatment of patients with refractory rheumatoid arthritis, but its value as an intervention therapy is limited by its toxicity.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1002/art.1780300102

Cyclosporin A Treatment of Refractory Rheumatoid Arthritis

The effect of cyclosporine of renal function in newly diagnosed diabetics.

In November 1982 a “pilot” (uncontrolled) clinical trial of the effects of the administration of ciclosporin to volunteer subjects with recent onset Type I diabetes mellitus was initiated. The rationale and preliminary findings in this study have been published earlier [1]. In this presentation we summarize further experience in this ongoing trial.

Effects of Ciclosporin on Insulin Secretion in Recent Onset Type I Diabetes Mellitus

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

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Papers

The effect of cyclosporine of renal function in newly diagnosed diabetics.

Effects of Ciclosporin on Insulin Secretion in Recent Onset Type I Diabetes Mellitus

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