Evidence map›Paper›PMID 32808093›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2020

Role of the IL-2 inducible tyrosine kinase ITK and its inhibitors in disease pathogenesis.

Kristina S Lechner, Markus F Neurath, Benno Weigmann

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2020. 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
3.0field-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, 67 citations in OpenAlex.

  1. CD14Frontiers in immunology · 2025
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  18. Covalent targeting of splicing in T cells.Cell chemical biology · 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

3 authors at 1 institution in 1 country.

Kristina S LechnerDepartment of Medicine 1, Kussmaul Campus for Medical Research, University of Erlangen-Nürnberg, Hartmannstr.14, 91052, Erlangen, Germany.
Markus F NeurathDepartment of Medicine 1, Kussmaul Campus for Medical Research, University of Erlangen-Nürnberg, Hartmannstr.14, 91052, Erlangen, Germany.
Benno WeigmannDepartment of Medicine 1, Kussmaul Campus for Medical Research, University of Erlangen-Nürnberg, Hartmannstr.14, 91052, Erlangen, Germany. Benno.Weigmann@uk-erlangen.de.ORCID 0000-0002-2398-0844
Friedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ITK (IL-2-inducible tyrosine kinase) belongs to the Tec family kinases and is mainly expressed in T cells. It is involved in TCR signalling events driving processes like T cell development as well as Th2, Th9 and Th17 responses thereby controlling the expression of pro-inflammatory cytokines. Studies have shown that ITK is involved in the pathogenesis of autoimmune diseases as well as in carcinogenesis. The loss of ITK or its activity either by mutation or by the use of inhibitors led to a beneficial outcome in experimental models of asthma, inflammatory bowel disease and multiple sclerosis among others. In humans, biallelic mutations in the ITK gene locus result in a monogenetic disorder leading to T cell dysfunction; in consequence, mainly EBV infections can lead to severe immune dysregulation evident by lymphoproliferation, lymphoma and hemophagocytic lymphohistiocytosis. Furthermore, patients who suffer from angioimmunoblastic T cell lymphoma have been found to express significantly more ITK. These findings put ITK in the strong focus as a target for drug development.

Indexed as

Disease SusceptibilityAnimalsAutoimmune DiseasesBiomarkersHumansInflammationInterleukin-2NeoplasmsProtein Kinase InhibitorsProtein-Tyrosine KinasesBiomarkersemt protein-tyrosine kinaseInterleukin-2Protein Kinase InhibitorsProtein-Tyrosine KinasesAutoimmune diseasesCancerInhibitorITK

Identifiers

PMID32808093
PMCPMC7524833
OpenAlexW3072700099

What Socratic 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 Socratic graph.