Evidence map›Paper›PMID 27318947›Full record

ReviewClinical reviews in allergy & immunology2017

Regulatory T Cells in Systemic Sclerosis: a Comprehensive Review.

Gleb Slobodin, Doron Rimar

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.4field-weighted citation impact, top 4% 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, 51 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Gleb SlobodinRheumatology, Bnai Zion Medical Center, Haifa, Israel. gslobodin@yahoo.com.
Doron RimarRheumatology, Bnai Zion Medical Center, Haifa, Israel.
Bnai Zion Medical Center · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic sclerosis (SSc) is a chronic inflammatory disease with complex pathogenesis, based on the sophisticated interplay of injury to the vascular endothelium, exaggerated tissue regeneration and fibrosis, and extensive immune abnormalities. The role of regulatory T cells (Tregs) in the development of SSc has started being studied during the last decade with new aspects being disclosed continuously, in parallel with the better understanding of Tregs physiology. There is a general agreement in the medical literature regarding the decreased functional capacity of circulating Tregs in SSc. Some patients, particularly those with active disease, may have increased numbers of circulating Tregs, representing the inhibitory response of the immune system to its inappropriate activation or occurring as a compensatory move for Tregs' decreased suppressive ability. Decreased pool of circulating Tregs can be seen in other SSc patients, with even lower Treg percentages seen in patients with long-standing disease. Skin-resident Tregs are depleted in advanced SSc but can be active and have a role in earlier disease stages. In addition to diminished suppressive ability, Tregs can contribute to SSc evolution by their microenvironment-dependent transformation to pathogenic effector T cells of Th17 or Th2 lineages with respective pro-inflammatory or pro-fibrotic activity. The current data on the effects of existing treatment modalities, including autologous stem cell transplantation, on Tregs function in SSc, is controversial, not being sufficiently elaborated.

Indexed as

HumansScleroderma, SystemicT-Lymphocytes, RegulatoryRegulatory T cellsSkin-resident regulatory T cellsSystemic sclerosis

Identifiers

PMID27318947
OpenAlexW2436882296

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.