Evidence map›Paper›PMID 29559975›Full record

ReviewFrontiers in immunology2018

TANK-Binding Kinase 1-Dependent Responses in Health and Autoimmunity.

Cynthia Louis, Chris Burns, Ian Wicks

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

43 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
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  16. Review
  17. Identification of 1Journal of enzyme inhibition and medicinal chemistry · 2022
    Article
  18. The RING finger protein family in health and disease.Signal transduction and targeted therapy · 2022
    Review
  19. Mechanisms of Antiviral Immune Evasion of SARS-CoV-2.Journal of molecular biology · 2022
    Review
  20. Article
4 · The record

Corrections and comments

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

3 authors at 2 institutions in 1 country.

Cynthia LouisInflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.
Chris BurnsChemical Biology Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.
Ian WicksInflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.
Walter and Eliza Hall Institute of Medical Research · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of autoimmune diseases, such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) is driven by genetic predisposition and environmental triggers that lead to dysregulated immune responses. These include the generation of pathogenic autoantibodies and aberrant production of inflammatory cytokines. Current therapies for RA and other autoimmune diseases reduce inflammation by targeting inflammatory mediators, most of which are innate response cytokines, resulting in generalized immunosuppression. Overall, this strategy has been very successful, but not all patients respond, responses can diminish over time and numerous side effects can occur. Therapies that target the germinal center (GC) reaction and/or antibody-secreting plasma cells (PC) potentially provide a novel approach. TANK-binding kinase 1 (TBK1) is an IKK-related serine/threonine kinase best characterized for its involvement in innate antiviral responses through the induction of type I interferons. TBK1 is also gaining attention for its roles in humoral immune responses. In this review, we discuss the role of TBK1 in immunological pathways involved in the development and maintenance of antibody responses, with particular emphasis on its potential relevance in the pathogenesis of humoral autoimmunity. First, we review the role of TBK1 in the induction of type I IFNs. Second, we highlight how TBK1 mediates inducible T cell co-stimulator signaling to the GC T follicular B helper population. Third, we discuss emerging evidence on the contribution of TBK1 to autophagic pathways and the potential implications for immune cell function. Finally, we discuss the therapeutic potential of TBK1 inhibition in autoimmunity.

Indexed as

AnimalsAutoantibodiesAutoimmune DiseasesAutoimmunityGene-Environment InteractionGenetic Predisposition to DiseaseHumansImmunity, HumoralMolecular Targeted TherapyPlasma CellsProtein Serine-Threonine KinasesVirus DiseasesAutoantibodiesProtein Serine-Threonine KinasesTBK1 protein, humanautoimmunityautophagygerminal centerhumoral immunityTANK-binding kinase 1type 1 interferons

Identifiers

PMID29559975
PMCPMC5845716
OpenAlexW2789542989

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.