Evidence map›Paper›PMID 30482489›Full record

ReviewCellular immunology2019

Restoring self-tolerance in autoimmune diseases by enhancing regulatory T-cells.

Prabhakaran Kumar, Shikha Saini, Saad Khan, Swarali Surendra Lele, Bellur S Prabhakar

Open access · greenAbstract readReview
In one paragraph

Review in Cellular immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
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  6. Yerba Mate (Nutrients · 2025
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  7. Rac1 overexpression promotes Treg-derived cytokines to mediate choroidal neovascularization in wet age-related macular degeneration.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 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

5 authors at 3 institutions in 1 country.

Prabhakaran KumarDepartment of Microbiology and Immunology, University of Illinois - College of Medicine, Chicago, IL, USA.
Shikha SainiDepartment of Microbiology and Immunology, University of Illinois - College of Medicine, Chicago, IL, USA.
Saad KhanDepartment of Microbiology and Immunology, University of Illinois - College of Medicine, Chicago, IL, USA.
Swarali Surendra LeleDepartment of Microbiology and Immunology, University of Illinois - College of Medicine, Chicago, IL, USA.
Bellur S PrabhakarDepartment of Microbiology and Immunology, University of Illinois - College of Medicine, Chicago, IL, USA. Electronic address: bprabhak@uic.edu.
Illinois College · USUniversity of Illinois Chicago · USUniversity of Illinois Urbana-Champaign · US

Funding

G-BMDC-induced Treg mediated suppression of Type 1 Diabetes in NOD miceR01AI107516 · NIAID · UNIVERSITY OF ILLINOIS AT CHICAGO · PI PRABHAKAR, BELLUR S · 2014 to 2017
$1.6M
NIAID NIH HHS R01 AI107516
6 · The paper itself

Abstract

Self-tolerance, the state of unresponsiveness to self-tissues/antigens, is maintained through central and peripheral tolerance mechanisms, and a breach of these mechanisms leads to autoimmune diseases. Foxp3 + T-regulatory cells (Tregs) play an essential role in suppressing autoimmune response directed against self-antigens and thereby regulate self-tolerance. Natural Tregs are differentiated in the thymus on the basis of their higher TCR-affinity to self-antigens and migrate to the periphery where they maintain peripheral tolerance. In addition, extra-thymic differentiation of induced Tregs can occur in the periphery which can control abrupt immune responses under inflammatory conditions. A defect in Treg cell numbers and/or function is found to be associated with the development of autoimmune disease in several experimental models and human autoimmune diseases. Moreover, augmentation of Tregs has been shown to be beneficial in treating autoimmunity in preclinical models, and Treg based cellular therapy has shown initial promise in clinical trials. However, emerging studies have identified an unstable subpopulation of Tregs which expresses pro-inflammatory cytokines under both homeostatic and autoimmune conditions, as well as in ex vivo cultures. In addition, clinical translation of Treg cellular therapy is impeded by limitations such as lack of easier methods for selective expansion of Tregs and higher cost associated with GMP-facilities required for cell sorting, ex vivo expansion and infusion of ex vivo expanded Tregs. Here, we discuss the recent advances in molecular mechanisms regulating Treg differentiation, Foxp3 expression and lineage stability, the role of Tregs in the prevention of various autoimmune diseases, and critically review their clinical utility for treating human autoimmune diseases.

Indexed as

AnimalsAutoimmune DiseasesAutoimmunityCell DifferentiationHumansSelf ToleranceT-Lymphocytes, RegulatoryAutoimmunityFoxp3 expressionImmune toleranceTreg differentiationTreg immunotherapy

Identifiers

PMID30482489
PMCPMC6440877
OpenAlexW2892567672

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.