Document Detail


RAGE-independent autoreactive B cell activation in response to chromatin and HMGB1/DNA immune complexes.
MedLine Citation:
PMID:  20014975     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Increasing evidence suggests that the excessive accumulation of apoptotic or necrotic cellular debris may contribute to the pathology of systemic autoimmune disease. HMGB1 is a nuclear DNA-associated protein, which can be released from dying cells thereby triggering inflammatory processes. We have previously shown that IgG2a-reactive B cell receptor (BCR) transgenic AM14 B cells proliferate in response to endogenous chromatin immune complexes (ICs), in the form of the anti-nucleosome antibody PL2-3 and cell debris, in a TLR9-dependent manner, and that these ICs contain HMGB1. Activation of AM14 B cells by these chromatin ICs was inhibited by a soluble form of the HMGB1 receptor, RAGE-Fc, suggesting HMGB1-RAGE interaction was important for this response. To further explore the role of HMGB1 in autoreactive B cell activation, we assessed the capacity of purified calf thymus HMGB1 to bind dsDNA fragments and found that HMGB1 bound both CG-rich and CG-poor DNA. However, HMGB1-DNA complexes could not activate AM14 B cells unless HMGB1 was bound by IgG2a and thereby able to engage the BCR. To ascertain the role of RAGE in autoreactive B cell responses to chromatin ICs, we intercrossed AM14 and RAGE-deficient mice. We found that spontaneous and defined DNA ICs activated RAGE+ and RAGE(- ) AM14 B cells to a comparable extent. These results suggest that HMGB1 promotes B cell responses to endogenous TLR9 ligands through a RAGE-independent mechanism.
Authors:
Ana M Avalos; Kerstin Kiefer; Jane Tian; Sean Christensen; Mark Shlomchik; Anthony J Coyle; Ann Marshak-Rothstein
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Autoimmunity     Volume:  43     ISSN:  1607-842X     ISO Abbreviation:  Autoimmunity     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-01-20     Completed Date:  2010-03-18     Revised Date:  2012-10-09    
Medline Journal Info:
Nlm Unique ID:  8900070     Medline TA:  Autoimmunity     Country:  England    
Other Details:
Languages:  eng     Pagination:  103-10     Citation Subset:  IM    
Affiliation:
Department of Microbiology, Boston University School of Medicine, Boston, MA 02118, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigen-Antibody Complex / immunology
Autoimmune Diseases / immunology*
B-Lymphocytes / immunology*
Cell Proliferation
Chromatin / immunology
DNA / immunology*
Flow Cytometry
HMGB1 Protein / immunology*
Lymphocyte Activation / immunology*
Mice
Mice, Knockout
Mice, Transgenic
Mitogen-Activated Protein Kinases / deficiency,  immunology*
Receptors, Antigen, B-Cell / immunology*
Toll-Like Receptor 9 / immunology
Grant Support
ID/Acronym/Agency:
P01 AR050256/AR/NIAMS NIH HHS; P01 AR050256-06/AR/NIAMS NIH HHS; R01 AI073722-04/AI/NIAID NIH HHS; R01 AR035230/AR/NIAMS NIH HHS; R01 AR035230-24/AR/NIAMS NIH HHS
Chemical
Reg. No./Substance:
0/Antigen-Antibody Complex; 0/Chromatin; 0/HMGB1 Protein; 0/Receptors, Antigen, B-Cell; 0/Tlr9 protein, mouse; 0/Toll-Like Receptor 9; 9007-49-2/DNA; EC 2.7.1.-/Stk30 protein, mouse; EC 2.7.11.24/Mitogen-Activated Protein Kinases
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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