NDLI: B lymphocyte 'original sin' in the bone marrow enhances islet autoreactivity in type 1 diabetes-prone nonobese diabetic mice.

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B lymphocyte 'original sin' in the bone marrow enhances islet autoreactivity in type 1 diabetes-prone nonobese diabetic mice.

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B lymphocyte 'original sin' in the bone marrow enhances islet autoreactivity in type 1 diabetes-prone nonobese diabetic mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Karamali, Mariam Rachakonda, Amita B. Henry-Bonami, Rachel A. Thomas, James W. Williams, Jonathan M. Kendall, Peggy L.
Description	Country affiliation: United States Author Affiliation: Henry-Bonami RA ( Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville TN 37232, USA.)
Abstract	Effective central tolerance is required to control the large extent of autoreactivity normally present in the developing B cell repertoire. Insulin-reactive B cells are required for type 1 diabetes in the NOD mouse, because engineered mice lacking this population are protected from disease. The Cg-Tg(Igh-6/Igh-V125)2Jwt/JwtJ (VH125Tg) model is used to define this population, which is found with increased frequency in the periphery of NOD mice versus nonautoimmune C57BL/6 VH125Tg mice; however, the ontogeny of this disparity is unknown. To better understand the origins of these pernicious B cells, anti-insulin B cells were tracked during development in the polyclonal repertoire of VH125Tg mice. An increased proportion of insulin-binding B cells is apparent in NOD mice at the earliest point of Ag commitment in the bone marrow. Two predominant L chains were identified in B cells that bind heterologous insulin. Interestingly, Vκ4-57-1 polymorphisms that confer a CDR3 Pro-Pro motif enhance self-reactivity in VH125Tg/NOD mice. Despite binding circulating autoantigen in vivo, anti-insulin B cells transition from the parenchyma to the sinusoids in the bone marrow of NOD mice and enter the periphery unimpeded. Anti-insulin B cells expand at the site of autoimmune attack in the pancreas and correlate with increased numbers of IFN-Î³-producing cells in the repertoire. These data identify the failure to cull autoreactive B cells in the bone marrow as the primary source of anti-insulin B cells in NOD mice and suggest that dysregulation of central tolerance permits their escape into the periphery to promote disease.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1201359
Journal	The Journal of Immunology
Issue Number	12
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Autoimmunity Immunology B-lymphocytes Bone Marrow Cells Diabetes Mellitus, Type 1 Islets Of Langerhans Self Tolerance Amino Acid Sequence Animals Autoantigens Cell Separation Enzyme-linked Immunosorbent Assay Flow Cytometry Immunoglobulin Variable Region Chemistry Genetics Insulin Lymphocyte Activation Mice Mice, Inbred Nod Molecular Sequence Data Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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