Evidence map›Paper›PMID 31082431›Full record

ReviewPharmacology & therapeutics2019

Non-receptor tyrosine kinase signaling in autoimmunity and therapeutic implications.

Sabrina Solouki, Avery August, Weishan Huang

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

22 citing papers in PubMed, 27 citations in OpenAlex.

  1. Atopic Dermatitis: New Targets and Emerging Systemic Therapies.American journal of clinical dermatology · 2026
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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.

Sabrina SoloukiDepartment of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
Avery AugustDepartment of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA. Electronic address: averyaugust@cornell.edu.
Weishan HuangDepartment of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA; Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803, USA. Electronic address: huang1@lsu.edu.
Cornell University · US

Funding

The role of adipocyte-driven inflammation and leptin pathway in pulmonary viral infections caused by SARS-CoV-2 and influenza A virusesP20GM130555 · NIGMS · LOUISIANA STATE UNIV A&M COL BATON ROUGE · PI Stephania A Cormier, TAMMY R DUGAS · 2019 to 2026
$19.9M
Protein CoreP30GM110760 · NIGMS · LOUISIANA STATE UNIV A&M COL BATON ROUGE · PI BAINES, JOEL D. · 2014 to 2018
$5.6M
Regulation of IL10 production in CD8+ T cells during Flu infection by tyrosine kinase ItkR01AI138570 · NIAID · CORNELL UNIVERSITY · PI AUGUST, AVERY · 2018 to 2022
$2.1M
Itk mediated tuning of CD8+ memory T cell developmentR01AI120701 · NIAID · CORNELL UNIVERSITY · PI AUGUST, AVERY · 2016 to 2019
$1.5M
A novel murine model of allergic airway inflammation.R21AI138497 · NIAID · CORNELL UNIVERSITY · PI AUGUST, AVERY, HUANG, WEISHAN · 2018 to 2019
$443k
Itk signaling and Type 1 regulatory T cell differentiation and function in allergic airway inflammationR21AI129422 · NIAID · CORNELL UNIVERSITY · PI AUGUST, AVERY, HUANG, WEISHAN · 2018 to 2019
$431k
Controlling Th17 cells and responses in airway inflammation by tyrosine kinase ItkR21AI126814 · NIAID · CORNELL UNIVERSITY · PI AUGUST, AVERY · 2016 to 2017
$426k
GCN2 signaling in pathogenic and regulatory T cell development in allergic airway inflammationR21AI137822 · NIAID · LOUISIANA STATE UNIV A&M COL BATON ROUGE · PI HUANG, WEISHAN · 2018 to 2019
$407k
Howard Hughes Medical InstituteNIAID NIH HHS R01 AI120701NIAID NIH HHS R01 AI138570NIAID NIH HHS R21 AI126814NIAID NIH HHS R21 AI129422NIAID NIH HHS R21 AI137822NIAID NIH HHS R21 AI138497NIGMS NIH HHS P20 GM130555NIGMS NIH HHS P30 GM110760
6 · The paper itself

Abstract

Autoimmune diseases are characterized by impaired immune tolerance towards self-antigens, leading to enhanced immunity to self by dysfunctional B cells and/or T cells. The activation of these cells is controlled by non-receptor tyrosine kinases (NRTKs), which are critical mediators of antigen receptor and cytokine receptor signaling pathways. NRTKs transduce, amplify and sustain activating signals that contribute to autoimmunity, and are counter-regulated by protein tyrosine phosphatases (PTPs). The function of and interaction between NRTKs and PTPs during the development of autoimmunity could be key points of therapeutic interference against autoimmune diseases. In this review, we summarize the current state of knowledge of the functions of NRTKs and PTPs involved in B cell receptor (BCR), T cell receptor (TCR), and cytokine receptor signaling pathways that contribute to autoimmunity, and discuss their targeting for therapeutic approaches against autoimmune diseases.

Indexed as

AnimalsAutoimmune DiseasesAutoimmunityHumansImmune ToleranceProtein-Tyrosine KinasesProtein Tyrosine PhosphatasesReceptors, Antigen, B-CellReceptors, Antigen, T-CellReceptors, CytokineSignal TransductionProtein-Tyrosine KinasesProtein Tyrosine PhosphatasesReceptors, Antigen, B-CellReceptors, Antigen, T-CellReceptors, CytokineAutoantibodiesAutoimmunityEffector T cellsKinase InhibitorsNon-receptor tyrosine kinaseProtein Tyrosine Phosphatase

Identifiers

PMID31082431
PMCPMC6738557
OpenAlexW2944583772

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.