Type 1 diabetes has long been thought of as a T cell–mediated disease. Now, a new study in mice makes a strong case that maternal autoantibodies can play an essential role in the initiation of diabetes. (pages 399–402)
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References
Greeley, S.A.W. et al. Elimination of maternally-transmitted autoantibodies prevents diabetes in nonobese diabetic mice. Nature Med. 8, 399–402 (2002).
Van Kerckhove, C. Lupus erythematosus in childhood: Effect of maternal factors beyond neonatal disease? Clin. Rheumatol. 9, 168–170 (1990).
Wrede, G., Kiesel, U., Freytag, G. & Kolb, H. Chronic insulitis after partial islet damage by passive insulin antibody transfer. Horm. Metab. Res. 16 (Suppl. 1), 97–101 (1984).
Bendelac, A., Carnaud, C., Boitard, C. & Bach, J.F. Syngeneic transfer of autoimmune diabetes from diabetic NOD mice to healthy neonates. Requirement for both L3T4+ and Lyt-2+ T cells. J. Exp. Med. 166, 823–832 (1987).
Bendelac, A. et al. Adoptive T cell transfer of autoimmune nonobese diabetic mouse diabetes does not require recruitment of host B lymphocytes. J. Immunol. 141, 2625–2628 (1988).
Marner, B. et al. Islet cell antibodies in insulin-dependent (Type 1) diabetic children treated with plasmapheresis. Diabetes. Res. 2, 231–236 (1985).
Andersson, A., Forsgren, S., Soderstrom, A. & Holmberg, D. Monoclonal, natural antibodies prevent development of diabetes in the non-obese diabetic (NOD) mouse. J. Autoimmun. 4, 733–742 (1991).
Forsgren, S., Andersson, A., Hillorn, V., Soderstrom, A. & Holmberg, D. Immunoglobulin-mediated prevention of autoimmune diabetes in the non-obese diabetic (NOD) mouse. Scand. J. Immunol. 34, 445–451 (1991).
Luan, J.J. et al. Defective FcγRII gene expression in macrophages of NOD mice—Genetic linkage with up-regulation of IgG1 and IgG2b in serum. J. Immunol. 157, 4707–4716 (1996).
Naserke, H.E., Bonifacio, E. & Ziegler, A.G. Prevalence, characteristics and diabetes risk associated with transient maternally acquired islet antibodies and persistent islet antibodies in offspring of parents with Type 1 diabetes. J. Clin. Endocrinol. Metab. 86, 4826–4833 (2001).
Warram, J.H., Krolewski, A.S., Gottlieb, M.S. & Kahn, C.R. Differences in risk of insulin-dependent diabetes in offspring of diabetic mothers and diabetic fathers. N. Engl. J. Med. 311, 149–152 (1984).
Rulli, M. & Simell, O. Avidity of islet cell autoantibodies in non-diabetic children and children with insulin-dependent diabetes. Autoimmunity 31, 187–193 (1999).
Seewaldt, S. et al. Virus-induced autoimmune diabetes—Most β-cells die through inflammatory cytokines and not perforin from autoreactive (anti-viral) cytotoxic T-lymphocytes. Diabetes 49, 1801–1809 (2000).
Martin, S. et al. Brief report—Development of Type 1 diabetes despite severe hereditary B-cell deficiency. N. Engl. J. Med. 345, 1036–1040 (2001).
Holz, A. et al. Neither B lymphocytes nor antibodies directed against self antigens of the islets of Langerhans are required for development of virus-induced autoimmune diabetes. J. Immunol. 165, 5945–5953 (2000).
Serreze, D.V. et al. B lymphocytes are critical antigen-presenting cells for the initiation of T cell–mediated autoimmune diabetes in nonobese diabetic mice. J. Immunol. 161, 3912–3918 (1998).
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von Herrath, M., Bach, JF. Juvenile autoimmune diabetes: A pathogenic role for maternal antibodies?. Nat Med 8, 331–333 (2002). https://doi.org/10.1038/nm0402-331
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DOI: https://doi.org/10.1038/nm0402-331
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