Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

TLR9 Deficiency Leads to Accelerated Renal Disease and Myeloid Lineage Abnormalities in Pristane-Induced Murine Lupus

29 Jun 2016

Abstract excerpt

Systemic lupus erythematosus (SLE) is a chronic, life-threatening autoimmune disorder, leading to multiple organ pathologies and kidney destruction. Analyses of numerous murine models of spontaneous SLE have revealed a critical role for endosomal TLRs in the production of autoantibodies and development of other clinical disease manifestations. Nevertheless, the corresponding TLR9-deficient autoimmune-prone...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Immune Response and Inflammation
Share to Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Share to Systemic Lupus Erythematosus Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 27354219
DOI: 10.4049/jimmunol.1501943

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

TLR9 Deficiency Leads to Accelerated Renal Disease and Myeloid Lineage Abnormalities in Pristane-Induced Murine LupusPMID 27354219Read ↗

Critical role of TLR2 and TLR4 in autoantibody production and glomerulonephritis in lpr mutation-induced mouse lupus.Semantic proximity Read ↗

Sustained NPSLE-like phenotype in the absence of systemic lupus-like disease in TLR7-deficient B6.Nba2 mice.Semantic proximity Read ↗

Exacerbated Autoimmunity in the Absence of TLR9 in MRL. <i>Faslpr</i> Mice Depends on <i>Ifnar1</i>Semantic proximity Read ↗

B cell-intrinsic TLR7 expression drives severe lupus in TLR9-deficient mice.Semantic proximity Read ↗

Immune cell alterations in a pristane‐induced lupus model in C57BL/6J miceSemantic proximity Read ↗

Type I interferon receptor controls B-cell expression of nucleic acid-sensing Toll-like receptors and autoantibody production in a murine model of lupusSemantic proximity Read ↗

Toll-like receptor 9 suppresses lupus disease in Fas-sufficient MRL Mice.Semantic proximity Read ↗

Phenotypic and functional alterations of pDCs in lupus-prone mice.Semantic proximity Read ↗

TLR9 Regulates TLR7- and MyD88-Dependent Autoantibody Production and Disease in a Murine Model of LupusSemantic proximity Read ↗

Opposing Impact of B Cell–Intrinsic TLR7 and TLR9 Signals on Autoantibody Repertoire and Systemic InflammationSemantic proximity Read ↗

A Toll for lupusSemantic proximity Read ↗

Human and Murine Toll-like Receptor-Driven Disease in Systemic Lupus Erythematosus.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.