Evidence map›Paper›PMID 32026417›Full record

ReviewAdvances in experimental medicine and biology2021

Interleukin-36: Structure, Signaling and Function.

Li Zhou, Viktor Todorovic

Abstract readReview
PubMed Publisher
In one paragraph

Review in Advances in experimental medicine and biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
18.7field-weighted citation impact, top 1% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Inflammation and Psoriasis: A Comprehensive Review.International journal of molecular sciences · 2023
    Review
  13. Article
  14. Correlations between IL-36 family cytokines in peripheral blood and subjective and objective assessment results in patients with allergic rhinitis.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2023
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Targeting IL-36 in Inflammatory Skin Diseases.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2023
    Article
  20. Dermatologic Manifestations of Noninflammasome-Mediated Autoinflammatory Diseases.JID innovations : skin science from molecules to population health · 2023
    Review
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

2 authors at 1 institution in 1 country.

Li Zhou *AbbVie Bioresearch Center, Worcester, MA, USA. li.zhou@abbvie.com.
Viktor Todorovic *AbbVie Inc., North Chicago, IL, USA.
AbbVie (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The IL-36 family belongs to a larger IL-1 superfamily and consists of three agonists (IL-36α/β/γ), one antagonist (IL-36Ra), one cognate receptor (IL-36R) and one accessory protein (IL-1RAcP). The receptor activation follows a two-step mechanism in that the agonist first binds to IL-36R and the resulting binary complex recruits IL-1RAcP. Assembled ternary complex brings together intracellular TIR domains of receptors which activate downstream NF-κB and MAPK signaling. Antagonist IL-36Ra inhibits the signaling by binding to IL-36R and preventing recruitment of IL-1RAcP. Members of IL-36 are normally expressed at low levels. Upon stimulation, they are inducted and act on a variety of cells including epithelial and immune cells. Protease mediated N-terminal processing is needed for cytokine activation. In the skin, the functional role of IL-36 is to contribute to host defense through inflammatory response. However, when dysregulated, IL-36 stimulates keratinocyte and immune cells to enhance the Th17/Th23 axis and induces psoriatic-like skin disorder. Genetic mutations of the antagonist IL-36Ra are associated with occurrence of generalized pustular psoriasis, a rare but life-threatening skin disease. Anti-IL-36 antibodies attenuate IMQ or IL-23 induced skin inflammation in mice, illustrating IL-36's involvement in mouse model of psoriasis. Other organs such as the lungs, the intestine, the joints and the brain also express IL-36 family members upon stimulation. The physiological and pathological roles of IL-36 are less well defined in these organs than in the skin. In this chapter, current progress on IL-36 protein and biology is reviewed with a discussion on investigative tools for this novel target.

Indexed as

Interleukin-1PsoriasisAnimalsInterleukin-1 Receptor Accessory ProteinInterleukinsMiceSkinInterleukin-1Interleukin-1 Receptor Accessory ProteinInterleukinsGeneralized pustular psoriasisIL-1 superfamilyIL-36InflammationPsoriasisTherapeutics

Identifiers

PMID32026417
OpenAlexW3004842828

What OpenQuestion holds

Textmetadata
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.