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K Fosgerau Rheoscience, Department of Infectious Diseases, Department of Clinical Immunology, Department of International Health, Steno Diabetes Center, Faculty of Health Sciences, Department of In Vivo Pharmacology, 2730 Herlev, Denmark

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P Galle Rheoscience, Department of Infectious Diseases, Department of Clinical Immunology, Department of International Health, Steno Diabetes Center, Faculty of Health Sciences, Department of In Vivo Pharmacology, 2730 Herlev, Denmark

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T Hansen Rheoscience, Department of Infectious Diseases, Department of Clinical Immunology, Department of International Health, Steno Diabetes Center, Faculty of Health Sciences, Department of In Vivo Pharmacology, 2730 Herlev, Denmark

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A Albrechtsen Rheoscience, Department of Infectious Diseases, Department of Clinical Immunology, Department of International Health, Steno Diabetes Center, Faculty of Health Sciences, Department of In Vivo Pharmacology, 2730 Herlev, Denmark

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C de Lemos Rieper Rheoscience, Department of Infectious Diseases, Department of Clinical Immunology, Department of International Health, Steno Diabetes Center, Faculty of Health Sciences, Department of In Vivo Pharmacology, 2730 Herlev, Denmark
Rheoscience, Department of Infectious Diseases, Department of Clinical Immunology, Department of International Health, Steno Diabetes Center, Faculty of Health Sciences, Department of In Vivo Pharmacology, 2730 Herlev, Denmark

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B Klarlund Pedersen Rheoscience, Department of Infectious Diseases, Department of Clinical Immunology, Department of International Health, Steno Diabetes Center, Faculty of Health Sciences, Department of In Vivo Pharmacology, 2730 Herlev, Denmark

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L Kongskov Larsen Rheoscience, Department of Infectious Diseases, Department of Clinical Immunology, Department of International Health, Steno Diabetes Center, Faculty of Health Sciences, Department of In Vivo Pharmacology, 2730 Herlev, Denmark

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A Randrup Thomsen Rheoscience, Department of Infectious Diseases, Department of Clinical Immunology, Department of International Health, Steno Diabetes Center, Faculty of Health Sciences, Department of In Vivo Pharmacology, 2730 Herlev, Denmark

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O Pedersen Rheoscience, Department of Infectious Diseases, Department of Clinical Immunology, Department of International Health, Steno Diabetes Center, Faculty of Health Sciences, Department of In Vivo Pharmacology, 2730 Herlev, Denmark
Rheoscience, Department of Infectious Diseases, Department of Clinical Immunology, Department of International Health, Steno Diabetes Center, Faculty of Health Sciences, Department of In Vivo Pharmacology, 2730 Herlev, Denmark

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M Bagge Hansen Rheoscience, Department of Infectious Diseases, Department of Clinical Immunology, Department of International Health, Steno Diabetes Center, Faculty of Health Sciences, Department of In Vivo Pharmacology, 2730 Herlev, Denmark

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A Steensberg Rheoscience, Department of Infectious Diseases, Department of Clinical Immunology, Department of International Health, Steno Diabetes Center, Faculty of Health Sciences, Department of In Vivo Pharmacology, 2730 Herlev, Denmark

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Abstract

Interleukin-6 (IL6) is critically involved in inflammation and metabolism. About 1% of people produce IL6 autoantibodies (aAb-IL6) that impair IL6 signaling in vivo. We tested the hypothesis that the prevalence of such aAb-IL6 is increased in type 2 diabetic patients and that aAb-IL6 plays a direct role in causing hyperglycemia. In humans, the prevalence of circulating high-affinity neutralizing aAb-IL6 was 2.5% in the type 2 diabetic patients and 1% in the controls (odds ratio 2.5, 95% confidence interval 1.2–4.9, P=0.01). To test for the role of aAb-IL6 in causing hyperglycemia, such aAb-IL6 were induced in mice by a validated vaccination procedure. Mice with plasma levels of aAb-IL6 similar to the 2.5% type 2 diabetic patients developed obesity and impaired glucose tolerance (area under the curve (AUC) glucose, 2056±62 vs 1793±62, P=0.05) as compared with sham-vaccinated mice, when challenged with a high-fat diet. Mice with very high plasma levels of aAb-IL6 developed elevated fasting plasma glucose (mM, 4.8±0.4 vs 3.3±0.1, P<0.001) and impaired glucose tolerance (AUC glucose, 1340±38 vs 916±25, P<0.001) as compared with sham-control mice on normal chow. In conclusion, the prevalence of plasma aAb-IL6 at levels known to impair IL6 signaling in vivo is increased 2.5-fold in people with type 2 diabetes. In mice, matching levels of aAb-IL6 cause obesity and hyperglycemia. These data suggest that a small subset of type 2 diabetes may in part evolve from an autoimmune attack against IL6.

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