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• W2101789045 abstract "Although autoantibodies (auto-Abs) against β-cell antigens helped in defining type 1 diabetes as an autoimmune disease and are invaluable biomarkers, their pathogenic role is unclear. Studies in nonobese diabetic (NOD) mice devoid of B cells ( Igμ null or treated with anti-μ Abs) suggest that B cells are necessary for the disease to develop (1,2). The critical role of B cells in this process is thought to be linked to their antigen-presenting function through major histocompatibility class II molecules, as NOD mice harboring I-Ag7–deficient B cells are also protected from diabetes (3). The capacity of B cells to efficiently uptake β-cell antigens through surface Ig is critical to this function, as inhibiting this Ig-mediated uptake abolishes the β-cell antigen-presenting function of B cells in vitro (4), while transgenic manipulation of the Ig specificity in NOD mice impacts on diabetes incidence (5). Thus, autoreactive B cells may be exquisitely efficient in capturing and presenting self antigens, leading to autoimmune T-cell activation. In a therapeutic perspective, treatment with depleting anti-CD20 Abs delays and reduces diabetes onset in NOD mice and is even capable of reversing established disease (6). These findings have been successfully translated into human clinical trials (7).In this scenario, the role of B cell–secreted auto-Abs has been controversial. On one hand, NOD embryos implanted into nonautoimmune foster mothers are diabetes-protected compared with embryos implanted into NOD females, suggesting that maternally transmitted factors (but not necessarily Abs) play a role (8). Moreover, passive transfer of Abs against islet-expressed …" @default.
• W2101789045 created "2016-06-24" @default.
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• W2101789045 date "2011-07-18" @default.
• W2101789045 modified "2023-10-17" @default.
• W2101789045 title "To B or Not to B: (Anti)bodies of Evidence on the Crime Scene of Type 1 Diabetes?" @default.
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• W2101789045 doi "https://doi.org/10.2337/db11-0700" @default.
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