NDLI: Opposing impact of B cell-intrinsic TLR7 and TLR9 signals on autoantibody repertoire and systemic inflammation.

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Opposing impact of B cell-intrinsic TLR7 and TLR9 signals on autoantibody repertoire and systemic inflammation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Liggitt, Denny Schwartz, Marc A. Rawlings, David J. Li, Quan-Zhen Alpers, Charles E. Scharping, Nicole E. Hudkins, Kelly L. Khim, Socheath Jackson, Shaun W. Kolhatkar, Nikita S.
Description	Author Affiliation: Jackson SW ( Department of Pediatrics, University of Washington School of Medicine, Seattle, WA 98195)
Abstract	Systemic lupus erythematosus is a multisystem autoimmune disease characterized by autoantibodies targeting nucleic acid-associated Ags. The endosomal TLRs TLR7 and TLR9 are critical for generation of Abs targeting RNA- or DNA-associated Ags, respectively. In murine lupus models, deletion of TLR7 limits autoimmune inflammation, whereas deletion of TLR9 exacerbates disease. Whether B cell or myeloid TLR7/TLR9 signaling is responsible for these effects has not been fully addressed. In this study, we use a chimeric strategy to evaluate the effect of B cell-intrinsic deletion of TLR7 versus TLR9 in parallel lupus models. We demonstrate that B cell-intrinsic TLR7 deletion prevents RNA-associated Ab formation, decreases production of class-switched Abs targeting nonnuclear Ags, and limits systemic autoimmunity. In contrast, B cell-intrinsic TLR9 deletion results in decreased DNA-reactive Ab, but increased Abs targeting a broad range of systemic autoantigens. Further, we demonstrate that B cell-intrinsic TLR9 deletion results in increased systemic inflammation and immune complex glomerulonephritis, despite intact TLR signaling within the myeloid compartment. These data stress the critical importance of dysregulated B cell-intrinsic TLR signaling in the pathogenesis of systemic lupus erythematosus.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1400098
Journal	The Journal of Immunology
Issue Number	10
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-05-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antibodies, Antinuclear Immunology B-lymphocytes Lupus Erythematosus, Systemic Membrane Glycoproteins Signal Transduction Toll-like Receptor 7 Toll-like Receptor 9 Animals Genetics Pathology Disease Models, Animal Inflammation Mice Mice, Knockout 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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Opposing impact of B cell intrinsic TLR7 and TLR9 signals on autoantibody repertoire and systemic inflammation

Toll-like receptors 7 and 9 regulate the proliferation and differentiation of B cells in systemic lupus erythematosus

Unbiased modifier screen reveals that signal strength determines the regulatory role murine TLR9 plays in autoantibody production.

Role of nucleic acid-sensing TLRs in diverse autoantibody specificities and anti-nuclear antibody-producing B cells.

Distinct Autoantibody Profiles in Systemic Lupus Erythematosus Patients are Selectively Associated with TLR7 and TLR9 Upregulation

TLR8 on dendritic cells and TLR9 on B cells restrain TLR7-mediated spontaneous autoimmunity in C57BL/6 mice

Up-Regulation of TLR7-Mediated IFN-α Production by Plasmacytoid Dendritic Cells in Patients With Systemic Lupus Erythematosus

B cell TLR7 expression drives anti-RNA autoantibody production and exacerbates disease in systemic lupus erythematosus-prone mice.

A Tlr7 translocation accelerates systemic autoimmunity in murine lupus.

Opposing impact of B cell-intrinsic TLR7 and TLR9 signals on autoantibody repertoire and systemic inflammation.

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Opposing impact of B cell intrinsic TLR7 and TLR9 signals on autoantibody repertoire and systemic inflammation

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Opposing impact of B cell-intrinsic TLR7 and TLR9 signals on autoantibody repertoire and systemic inflammation.