Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
3 · Its place in the literature
Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
15 authors at 1 institution in 2 countries.
Chelisa CardinezCentre for Personalised Immunology, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia.
Yuwei HaoCentre for Personalised Immunology, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia.ORCID 0000-0003-3932-3686
Kristy KwongCentre for Personalised Immunology, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia.ORCID 0000-0002-5675-0009
Ainsley R DaviesCentre for Personalised Immunology, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia.ORCID 0000-0003-3352-5578
Morgan B DownesCentre for Personalised Immunology, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia.ORCID 0009-0001-3784-6814
Nadia A RobertsDivision of Immunology and Infectious Diseases, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia.ORCID 0009-0004-4913-0495
Jason D PriceDivision of Genome Sciences and Cancer, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia.
Raquel A HernandezCentre for Personalised Immunology, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia.
Jessica LovellDivision of Immunology and Infectious Diseases, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia.
Rochna ChandCentre for Personalised Immunology, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia.
Zhi-Ping FengANU Bioinformatics Consultancy, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia.ORCID 0000-0002-6627-5934
Anselm EndersCentre for Personalised Immunology, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia.ORCID 0000-0001-5933-6463
Carola G VinuesaCentre for Personalised Immunology, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia.ORCID 0000-0001-9799-0298
Bahar MiraghazadehCentre for Personalised Immunology, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia.
Matthew C CookCentre for Personalised Immunology, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia. mc2386@cam.ac.uk.ORCID 0000-0002-3331-9363
Australian National University · AU
Funding
Department of Health | National Health and Medical Research Council (NHMRC) 1079648Department of Health | National Health and Medical Research Council (NHMRC) 1107464Department of Health | National Health and Medical Research Council (NHMRC) 1113577
6 · The paper itself
Abstract
Loss-of-function mutations have provided crucial insights into the immunoregulatory actions of Foxp3+ regulatory T cells (Tregs). By contrast, we know very little about the consequences of defects that amplify aspects of Treg function or differentiation. Here we show that mice heterozygous for an Ikbkb gain-of-function mutation develop psoriasis. Doubling the gene dose (Ikbkb
Indexed as
Gain of Function MutationI-kappa B KinaseT-Lymphocytes, RegulatoryAnimalsForkhead Transcription FactorsInflammationMiceForkhead Transcription FactorsI-kappa B KinaseIkbkb protein, mouse
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
IKK2 controls the inflammatory potential of tissue-resident regulatory T cells in a murine gain of function model. · full record | OpenQuestion