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Record W2519346478 · doi:10.1136/lupus-2016-000179.46

II-16 Protection of lupus nephritis by IRHOM2 deficiency in <i>FCRγIIB-/-</i> mice

2016· article· en· W2519346478 on OpenAlex

Why this work is in the frame

A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.

affAt least one author lists a Canadian institution in the pinned OpenAlex snapshot.

Bibliographic record

VenueInnate Immunity · 2016
Typearticle
Languageen
FieldMedicine
TopicMonoclonal and Polyclonal Antibodies Research
Canadian institutionsPrincess Margaret Cancer CentreUniversity Health Network
Fundersnot available
KeywordsLupus nephritisSystemic lupus erythematosusImmunologyKidneyMedicineGlomerulonephritisInternal medicineMolecular biologyBiology

Abstract

fetched live from OpenAlex

<h3>Background</h3> Lupus nephritis (LN) is a major cause of morbidity and mortality in lupus. A disintegrin and metalloprotease 17 (ADAM17), is a principal membrane-anchored metalloprotease that cleaves a large spectrum of membrane-bound proteins into their soluble forms. Inactive rhomboid protein 2 (iRhom2), a newly identified regulator of ADAM17, controls maturation and function of ADAM17. Interestingly, in iRhom2<sup>−</sup><sup>/<b>−</b></sup> mice, loss of ADAM17-dependent shedding activity is limited to the immune organs. Accumulating evidence has shown increased protein shedding and possibly activation of ADAM17 in lupus. Among ADAM17 substrates, tumour necrosis factor α (TNF-α) and heparin-binding EGF (HB-EGF) have been reported to play important roles in mediating renal damage in lupus. We hypothesised that the activation of iRhom2/ADAM17 pathway plays a role in the pathogenesis of lupus nephritis. <h3>Materials and methods</h3> We crossed <i>iRhom2<sup>−</sup><sup>/<b>−</b></sup></i> mice with the well-established <i>FcRγIIB-/-</i> lupus-prone mice, and assessed development of lupus-like syndrome in these mice. <h3>Results</h3> We found that <i>iRhom2</i> deficiency protects <i>FcRγIIB<sup>−</sup><sup>/<b>−</b></sup></i> mice from severe kidney damage (Figure 1), with minimal impact on the production of anti-double stranded (ds) DNA antibodies and renal deposition of immune complex and complement C3. In the absence of iRhom2, glomerular and tubule-interstitial structures were preserved, and massive inflammatory infiltrates including myeloid and CD4<sup>+</sup> T cells were alleviated in the lupus kidneys. Protection of kidney injury by <i>iRhom2</i> deficiency is associated with reduced EGFR signalling and ERK1/2 activation in the kidneys of <i>FcRγIIB<sup>−</sup><sup>/<b>−</b></sup></i> mice. Transcriptome analysis of the whole kidneys as well as kidney macrophages from <i>FcRγIIB<sup>−</sup><sup>/<b>−</b></sup></i> mice identified genes encoding pro-inflammatory cytokine/chemokines, fibrosis and tissue remodelling highly upregulated, and many of these genes were significantly reduced in the absence of <i>iRhom2</i>. In addition, kidney biopsies from patients with lupus nephritis show intense staining for HB-EGF, an EGFR ligand, in areas of crescents. <h3>Conclusions</h3> Our findings here provide the first evidence that iRhom2, a major regulator of ADAM17, plays a critical role in the pathogenesis of LN. The role of iRhom2 in a spontaneous chronic mouse model of LN, <i>FcRγIIB</i><sup>−</sup><sup>/<b>−</b></sup> mice, appears to be targeting at the effector arm of the disease, rather than affecting the process of autoimmunity development. iRhom2 may be a potential therapeutic target in LN. <h3>Acknowledgements</h3> Work supported by Lupus Research Institute (JES and CB) and Barbara Volcker Centre of Hospital for Special Surgery (XQ).

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

Full frame distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.194
Threshold uncertainty score0.999

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0000.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.023
GPT teacher head0.284
Teacher spread0.261 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it