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10.1084/jem.20151869

http://scihub22266oqcxt.onion/10.1084/jem.20151869
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suck abstract from ncbi


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pmid27139492
      J+Exp+Med 2016 ; 213 (6 ): 967-78
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  • Class-switched anti-insulin antibodies originate from unconventional antigen presentation in multiple lymphoid sites #MMPMID27139492
  • Wan X ; Thomas JW ; Unanue ER
  • J Exp Med 2016[May]; 213 (6 ): 967-78 PMID27139492 show ga
  • Autoantibodies to insulin are a harbinger of autoimmunity in type 1 diabetes in humans and in non-obese diabetic mice. To understand the genesis of these autoantibodies, we investigated the interactions of insulin-specific T and B lymphocytes using T cell and B cell receptor transgenic mice. We found spontaneous anti-insulin germinal center (GC) formation throughout lymphoid tissues with GC B cells binding insulin. Moreover, because of the nature of the insulin epitope recognized by the T cells, it was evident that GC B cells presented a broader repertoire of insulin epitopes. Such broader recognition was reproduced by activating naive B cells ex vivo with a combination of CD40 ligand and interleukin 4. Thus, insulin immunoreactivity extends beyond the pancreatic lymph node-islets of Langerhans axis and indicates that circulating insulin, despite its very low levels, can have an influence on diabetogenesis.
  • |Animals [MESH]
  • |Antigen Presentation/genetics/*immunology [MESH]
  • |B-Lymphocytes/*immunology/pathology [MESH]
  • |CD40 Antigens/genetics/immunology [MESH]
  • |Diabetes Mellitus, Type 1/genetics/*immunology/pathology [MESH]
  • |Germinal Center/*immunology/pathology [MESH]
  • |Immunoglobulin Class Switching/genetics/*immunology [MESH]
  • |Insulin/genetics/*immunology [MESH]
  • |Interleukin-4/genetics/immunology [MESH]
  • |Islets of Langerhans/immunology/pathology [MESH]
  • |Mice [MESH]
  • |Mice, Knockout [MESH]


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