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

Genetic susceptibility to polyI:C-induced IFNalpha/beta-dependent accelerated disease in lupus-prone mice.

Genes and immunity - 1 Oct 2006

Jørgensen T N, Thurman J, Izui S, Falta M T, Metzger T E, Flannery S A, Kappler J, Marrack P, Kotzin B L

Abstract excerpt

Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown etiology. Associations between viral infections and the onset of SLE have been suggested, and recent studies have provided evidence that type I interferons (IFNalpha/beta) might play a role in the SLE disease process. Viruses and interferons have also been implicated in mouse models of SLE. We generated a model of accelerated proteinuria, in...

Read the complete abstract on PubMed

Topics

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

Share to Antibodies, Antinuclear
Share to Immunoglobulin G

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Interferon-alpha

Share to Interferon-beta

Share to Kidney Glomerulus

Share to Lupus Nephritis

Share to Poly I-C

Share to Proteinuria

Source

Identifiers

PMID: 16900204
DOI: 10.1038/sj.gene.6364329

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Genetic susceptibility to polyI:C-induced IFNalpha/beta-dependent accelerated disease in lupus-prone mice.PMID 16900204Read ↗

Type I interferon signaling is involved in the spontaneous development of lupus-like disease in B6.Nba2 and (B6.Nba2 x NZW)F(1) mice.Semantic proximity Read ↗

IFNα Inducible Models of Murine SLESemantic proximity Read ↗

Interferon-alpha treatment of female (NZW x BXSB)F(1) mice mimics some but not all features associated with the Yaa mutation.Semantic proximity Read ↗

Assessing the Molecular Validity of Spontaneous Lupus Mouse Models and Its Implication for Human StudiesSemantic proximity Read ↗

CD8 T lymphocytes infiltrate the kidneys and correlate with disease progression in B6. <i>NZMSle1/Sle2/Sle3</i> lupus miceSemantic proximity Read ↗

IFN-alpha induces early lethal lupus in preautoimmune (New Zealand Black x New Zealand White) F1 but not in BALB/c mice.Semantic proximity Read ↗

Type-I Interferon Receptor Deficiency Reduces Lupus-like Disease in NZB MiceSemantic proximity Read ↗

Functional dissection of systemic lupus erythematosus using congenic mouse strains.Semantic proximity Read ↗

NZM2328: a new mouse model of systemic lupus erythematosus with unique genetic susceptibility loci.Semantic proximity Read ↗

Genetic Dissection of SLESemantic proximity Read ↗

Enhanced susceptibility to end-organ disease in the lupus-facilitating NZW mouse strain.Semantic proximity Read ↗

The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 MiceSemantic proximity Read ↗

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