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B cell selection defects underlie the development of diabetogenic apcs in nonobese diabetic mice

Academic Article
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Overview

authors

  • Nemazee, David
  • Serreze, D. V.
  • Chapman, H. D.
  • Dombrowsky, J.
  • Silveira, P. A.
  • Johnson, Ellis

publication date

  • April 2004

journal

  • Journal of Immunology  Journal

abstract

  • One mechanism whereby B cells contribute to type 1 diabetes in nonobese diabetic (NOD) mice is as a subset of APCs that preferentially presents MHC class II-bound pancreatic beta cell Ags to autoreactive CD4 T cells. This results from their ability to use cell surface Ig to specifically capture beta cell Ags. Hence, we postulated a diabetogenic role for defects in the tolerance mechanisms normally blocking the maturation and/or activation of B cells expressing autoreactive Ig receptors. We compared B cell tolerance mechanisms in NOD mice with nonautoimmune strains by using the IgHEL and Ig3-83 transgenic systems, in which the majority of B cells recognize one defined Ag. NOD- and nonautoimmune-prone mice did not differ in ability to delete or receptor edit B cells recognizing membrane-bound self Ags. However, in contrast to the nonautoimmune-prone background, B cells recognizing soluble self Ags in NOD mice did not undergo partial deletion and were also not efficiently anergized. The defective induction of B cell tolerance to soluble autoantigens is most likely responsible for the generation of diabetogenic APC in NOD mice.

subject areas

  • Animals
  • Antigen Presentation
  • Antigen-Presenting Cells
  • Autoantigens
  • B-Lymphocyte Subsets
  • Cell Differentiation
  • Clonal Anergy
  • Clonal Deletion
  • Diabetes Mellitus, Type 1
  • Female
  • Membrane Proteins
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred NOD
  • Mice, Transgenic
  • RNA Editing
  • Receptors, Antigen, T-Cell
  • Solubility
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Identity

PubMed Central ID

  • PMC3792717

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 15067092
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Additional Document Info

start page

  • 5086

end page

  • 5094

volume

  • 172

issue

  • 8

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