NDLI: Reversing Tolerance in Isotype Switch-Competent Anti-Insulin B Lymphocytes.

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Reversing Tolerance in Isotype Switch-Competent Anti-Insulin B Lymphocytes.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Bonami, Rachel H. Hulbert, Chrys Thomas, James W. Williams, Jonathan M.
Description	Author Affiliation: Williams JM ( Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, TN 37232); Bonami RH ( Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, TN 37232.); Hulbert C ( Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, TN 37232.); Thomas JW ( Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, TN 37232)
Abstract	Autoreactive B lymphocytes that escape central tolerance and mature in the periphery are a liability for developing autoimmunity. IgG insulin autoantibodies that predict type 1 diabetes and complicate insulin therapies indicate that mechanisms for tolerance to insulin are flawed. To examine peripheral tolerance in anti-insulin B cells, we generated C57BL/6 mice that harbor anti-insulin VDJH-125 site directed to the native IgH locus (VH125(SD)). Class switch-competent anti-insulin B cells fail to produce IgG Abs following T cell-dependent immunization of VH125(SD) mice with heterologous insulin, and they exhibit markedly impaired proliferation to anti-CD40 plus insulin in vitro. In contrast, costimulation with LPS plus insulin drives robust anti-insulin B cell proliferation. Furthermore, VH125(SD) mice produce both IgM and IgG2a anti-insulin Abs following immunization with insulin conjugated to type 1 T cell-independent Brucella abortus ring test Ag (BRT). Anti-insulin B cells undergo clonal expansion in vivo and emerge as IgM(+) and IgM(-) GL7(+)Fas(+) germinal center (GC) B cells following immunization with insulin-BRT, but not BRT alone. Analysis of Igκ genes in VH125(SD) mice immunized with insulin-BRT reveals that anti-insulin Vκ from the preimmune repertoire is selected into GCs. These data demonstrate that class switch-competent anti-insulin B cells remain functionally silent in T cell-dependent immune responses, yet these B cells are vulnerable to reversal of anergy following combined BCR/TLR engagement that promotes Ag-specific GC responses and Ab production. Environmental factors that lead to infection and inflammation could play a critical yet underappreciated role in driving loss of tolerance and promoting autoimmune disease.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1403114
Journal	The Journal of Immunology
Issue Number	3
Volume Number	195
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2015-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Autoantibodies Immunology B-lymphocytes Diabetes Mellitus, Type 1 Insulin Antibodies Insulin Animals Antigens, Cd40 Biosynthesis Autoimmunity Genetics Immune Tolerance Immunoglobulin G Immunoglobulin M Lipopolysaccharides Mice Mice, Inbred C57bl Mice, Transgenic Molecular Sequence Data Vdj Exons Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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