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Record W4401574918 · doi:10.1038/s41586-024-07820-3

Recognition and control of neutrophil extracellular trap formation by MICL

2024· article· en· W4401574918 on OpenAlexaff
Mariano Malamud, Lauren Whitehead, Alasdair McIntosh, Fabio Colella, Anke J. Roelofs, Takato Kusakabe, Ivy M. Dambuza, Annie Phillips-Brookes, Fabián Salazar, Federico M. Perez, Romey Shoesmith, Przemysław Zakrzewski, Emily A. Sey, Cecília Rodrigues, Petruta L. Morvay, Pierre Redelinghuys, Tina Bedekovic, Maria J. Fernandes, Ruqayyah J. Almizraq, Donald R. Branch, Borko Amulic, Jamie Harvey, Diane Stewart, Raif Yuecel, Delyth M. Reid, Alex McConnachie, Matthew C. Pickering, Marina Botto, Iliyan D. Iliev, Iain B. McInnes, Cosimo De Bari, Janet A. Willment, Gordon D. Brown

Bibliographic record

VenueNature · 2024
Typearticle
Languageen
FieldImmunology and Microbiology
TopicNeutrophil, Myeloperoxidase and Oxidative Mechanisms
Canadian institutionsCanadian Blood ServicesUniversité LavalHospital for Sick Children
FundersNational Institute of Allergy and Infectious DiseasesVersus ArthritisMedical Research CouncilNational Institutes of HealthUniversity of AberdeenUniversity of GlasgowNational Institute for Health and Care ResearchImperial College Healthcare NHS TrustImperial College LondonMedical Research Council Centre for Medical MycologyNational Institute of Diabetes and Digestive and Kidney DiseasesUniversity of ExeterWellcome Trust
KeywordsNeutrophil extracellular trapsTrap (plumbing)ExtracellularChemistryControl (management)Cell biologyBiologyInflammationPhysicsImmunologyComputer scienceArtificial intelligence

Abstract

fetched live from OpenAlex

Abstract Regulation of neutrophil activation is critical for disease control. Neutrophil extracellular traps (NETs), which are web-like structures composed of DNA and neutrophil-derived proteins, are formed following pro-inflammatory signals; however, if this process is uncontrolled, NETs contribute to disease pathogenesis, exacerbating inflammation and host tissue damage 1,2 . Here we show that myeloid inhibitory C-type lectin-like (MICL), an inhibitory C-type lectin receptor, directly recognizes DNA in NETs; this interaction is vital to regulate neutrophil activation. Loss or inhibition of MICL functionality leads to uncontrolled NET formation through the ROS–PAD4 pathway and the development of an auto-inflammatory feedback loop. We show that in the context of rheumatoid arthritis, such dysregulation leads to exacerbated pathology in both mouse models and in human patients, where autoantibodies to MICL inhibit key functions of this receptor. Of note, we also detect similarly inhibitory anti-MICL autoantibodies in patients with other diseases linked to aberrant NET formation, including lupus and severe COVID-19. By contrast, dysregulation of NET release is protective during systemic infection with the fungal pathogen Aspergillus fumigatus . Together, we show that the recognition of NETs by MICL represents a fundamental autoregulatory pathway that controls neutrophil activity and NET formation.

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.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation 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 score0.001
Threshold uncertainty score0.003

Distilled classifier scores by category (both heads)

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)0.0010.000

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 head0.010
GPT teacher head0.220
Teacher spread0.210 · 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

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations59
Published2024
Admission routes1
Has abstractyes

Explore more

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