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Finland and Sweden have the highest incidence of insulin-dependent diabetes in children in the world, about 3-4 times that of countries in the Mediterranean area, with the exception of Sardinia. We have collected information from several European clinics and from Pittsburgh, USA, in order to find out whether this difference incidence is associated with corresponding differences of the disease pattern. Patients in Finland or Sweden ('North') and Pittsburgh were younger (10 years old) at diagnosis compared with those in the other clinics in Europe (P0.05 versus P0.02). In the North, boys were in excess (58%) in contrast to France (40%) and Pittsburgh (46%). Patients in the North had a shorter duration of symptoms (8 days; P0.001) and higher blood glucose (20 mmol/l; P0.05) than those attending the other European clinics. Irrespective of age, there were more ICA-positive patients in the North (94%) than in Berlin-Vienna (67%; P0.01) or in France (70%; P0.01). There was a tendency for non-diabetic parents and siblings in the North to have lower C-peptide values (0.26 pmol/ml) at the time of diagnosis of the proband and to be ICA-positive more often than relatives in the other European clinics. The seasonal variation of diagnosis showed no obvious geographical differences, with recorded diagnosis always lowest during the summer. We conclude that certain factors seem to cause not only a high incidence of diabetes in children in Finland and Sweden but perhaps also a more aggressive early disease process.

In vivo-activated interleukin 2 receptor-positive T lymphocytes (Tac cells) are demonstrable and the autologous mixed leukocyte reaction (AMLR) is impaired in several autoimmune diseases, including type 1 insulin-dependent diabetes mellitus (IDDM). We investigated AMLR in greater detail, together with possible relationships between AMLR and Tac lymphocytes in IDDM. Coculture experiments with HLA identical patient-healthy sibling pairs revealed that both responder and stimulator cells of diabetic patients function abnormally in AMLR. Suppressive Tac lymphocytes among responder T cells seemed to impair their proliferation. The removal of Tac cells by immunomagnetic beads led to a striking enhancement of proliferation, while the restoration of AMLR cultures with enriched Tac cells was accompanied by a diminished response. The reasons for the poor stimulatory capacity of patient cells are at present unknown but may be due to altered function and/or structure of HLA-DR molecules.