NDLI: B cell-intrinsic TLR7 signaling is essential for the development of spontaneous germinal centers.

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B cell-intrinsic TLR7 signaling is essential for the development of spontaneous germinal centers.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Domeier, Phillip P. Wong, Eric B. Satoh, Takashi Rahman, Ziaur S. M. Soni, Chetna Khan, Tahsin N. Akira, Shizuo
Description	Author Affiliation: Soni C ( Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, PA 17033); Wong EB ( Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, PA 17033); Domeier PP ( Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, PA 17033); Khan TN ( Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, PA 17033); Satoh T ( Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan.); Akira S ( Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan.); Rahman ZS ( Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, PA 17033)
Abstract	Spontaneous germinal center (Spt-GC) B cells and follicular helper T cells generate high-affinity autoantibodies that are involved in the development of systemic lupus erythematosus. TLRs play a pivotal role in systemic lupus erythematosus pathogenesis. Although previous studies focused on the B cell-intrinsic role of TLR-MyD88 signaling on immune activation, autoantibody repertoire, and systemic inflammation, the mechanisms by which TLRs control the formation of Spt-GCs remain unclear. Using nonautoimmune C57BL/6 (B6) mice deficient in MyD88, TLR2, TLR3, TLR4, TLR7, or TLR9, we identified B cell-intrinsic TLR7 signaling as a prerequisite to Spt-GC formation without the confounding effects of autoimmune susceptibility genes and the overexpression of TLRs. TLR7 deficiency also rendered autoimmune B6.Sle1b mice unable to form Spt-GCs, leading to markedly decreased autoantibodies. Conversely, B6.yaa and B6.Sle1b.yaa mice expressing an extra copy of TLR7 and B6.Sle1b mice treated with a TLR7 agonist had increased Spt-GCs and follicular helper T cells. Further, TLR7/MyD88 deficiency led to compromised B cell proliferation and survival after B cell stimulation both in vitro and in vivo. In contrast, TLR9 inhibited Spt-GC development. Our findings demonstrate an absolute requirement for TLR7 and a negative regulatory function for TLR9 in Spt-GC formation under nonautoimmune and autoimmune conditions. Our data suggest that, under nonautoimmune conditions, Spt-GCs initiated by TLR7 produce protective Abs. However, in the presence of autoimmune susceptibility genes, TLR7-dependent Spt-GCs produce pathogenic autoantibodies. Thus, a single copy of TLR7 in B cells is the minimal requirement for breaking the GC-tolerance checkpoint.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1401720
Journal	The Journal of Immunology
Issue Number	9
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	B-lymphocytes Immunology Germinal Center Signal Transduction Toll-like Receptor 7 Metabolism Animals Antibody Formation Autoantibodies Autoimmunity Cell Survival Dendritic Cells Gene Expression Immunohistochemistry Immunophenotyping Lymphocyte Activation Mice Mice, Knockout Mice, Transgenic Phenotype T-lymphocyte Subsets Genetics Toll-like Receptor 9 Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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

Cell-intrinsic expression of TLR9 in autoreactive B cells constrains BCR/TLR7-dependent responses.

Leukocyte-associated Ig-like receptor-1-deficient mice have an altered immune cell phenotype.

TLR7- and TLR9-responsive human B cells share phenotypic and genetic characteristics.

Activation of rheumatoid factor-specific B cells is antigen dependent and occurs preferentially outside of germinal centers in the lupus-prone NZM2410 mouse model.

Cutting edge: Bcl6-interacting corepressor contributes to germinal center T follicular helper cell formation and B cell helper function.

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

B cell-intrinsic TLR7 signaling is essential for the development of spontaneous germinal centers

Toll-like receptor 9 signaling acts on multiple elements of the germinal center to enhance antibody responses.

B cell-intrinsic TLR7 signaling is essential for the development of spontaneous germinal centers.

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Leukocyte-associated Ig-like receptor-1-deficient mice have an altered immune cell phenotype.

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Activation of rheumatoid factor-specific B cells is antigen dependent and occurs preferentially outside of germinal centers in the lupus-prone NZM2410 mouse model.

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B cell-intrinsic TLR7 signaling is essential for the development of spontaneous germinal centers

Toll-like receptor 9 signaling acts on multiple elements of the germinal center to enhance antibody responses.

B cell-intrinsic TLR7 signaling is essential for the development of spontaneous germinal centers.