Evidence map›Paper›PMID 29247989›Full record

ReviewImmunological reviews2018

Tuning inflammation and immunity by the negative regulators IL-1R2 and IL-1R8.

Martina Molgora, Domenico Supino, Alberto Mantovani, Cecilia Garlanda

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
3.4field-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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.

  1. Pooled it
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  12. SIGIRR: An Orphan Receptor Mediating Anti-inflammatory Actions.Expert reviews in molecular medicine · 2025
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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

4 authors at 1 institution in 2 countries.

Martina MolgoraDepartment of Inflammation and Immunology, Humanitas Clinical and Research Center, Rozzano, Italy.ORCID 0000-0001-7328-2844
Domenico SupinoDepartment of Inflammation and Immunology, Humanitas Clinical and Research Center, Rozzano, Italy.ORCID 0000-0001-9690-1791
Alberto MantovaniDepartment of Inflammation and Immunology, Humanitas Clinical and Research Center, Rozzano, Italy.ORCID 0000-0001-5578-236X
Cecilia GarlandaDepartment of Inflammation and Immunology, Humanitas Clinical and Research Center, Rozzano, Italy.ORCID 0000-0002-1510-7703
Humanitas University · IT

Funding

European Research Council 669415
6 · The paper itself

Abstract

Interleukin-1 receptor family members (ILRs) and Toll-Like Receptors (TLRs) are key players in immunity and inflammation and are tightly regulated at different levels. Most cell types, including cells of the innate and adaptive immune system express ILRs and TLRs. In addition, IL-1 family members are emerging as key players in the differentiation and function of innate and adaptive lymphoid cells. IL-1R2 and IL-1R8 (also known as TIR8 or SIGIRR) are members of the ILR family acting as negative regulators of the IL-1 system. IL-1R2 binds IL-1 and the accessory protein IL-1RAcP without activating signaling and can be released as a soluble form (sIL-1R2), thus modulating IL-1 availability for the signaling receptor. IL-1R8 dampens ILR- and TLR-mediated cell activation and it is a component of the receptor recognizing human IL-37. Here, we summarize our current understanding of the structure and function of IL-1R2 and IL-1R8, focusing on their role in different pathological conditions, ranging from infectious and sterile inflammation, to autoimmunity and cancer-related inflammation. We also address the emerging evidence regarding the role of IL-1R8 as a crucial checkpoint molecule in NK cells in anti-cancer and antiviral activity and the potential therapeutic implications of IL-1R8 blockade in specific pathological contexts.

Indexed as

AnimalsHumansImmunityImmunologic SurveillanceImmunomodulationInfectionsInflammationKiller Cells, NaturalReceptors, Interleukin-1Receptors, Interleukin-1 Type IIIL1R2 protein, humanReceptors, Interleukin-1Receptors, Interleukin-1 Type IISIGIRR protein, humaninfectioninflammationinflammation-associated cancerinterleukin-1

Identifiers

PMID29247989
PMCPMC5922415
OpenAlexW2778693889

What OpenQuestion holds

Textmetadata
LicenceTDM
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.