Evidence map›Paper›PMID 34554499›Full record

ReviewBiologia futura2021

Biologia Futura: Emerging antigen-specific therapies for autoimmune diseases.

Gabriella Sármay

Open access · hybridAbstract readReview
PubMed Publisher
In one paragraph

Review in Biologia futura, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 35% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Impact of Siglecs on autoimmune diseases.Molecular aspects of medicine · 2023
    Review
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

1 author at 1 institution in 1 country.

Gabriella SármayDepartment of Immunology, Eötvös Loránd University, Budapest, Hungary. gabriella.sarmay@ttk.elte.hu.ORCID http://orcid.org/0000-0002-3066-7768
Eötvös Loránd University · HU

Funding

National Research Development and Innovation Office K 128546
6 · The paper itself

Abstract

Autoimmune diseases are caused by breaking the central and/or peripheral tolerance against self, leading to uncontrolled immune response to autoantigens. The incidences of autoimmune diseases have increased significantly worldwide over the last decades; nearly 5% of the world's population is affected. The current treatments aim to reduce pain and inflammation to prevent organ damage and have a general immunosuppressive effect, but they cannot cure the disease. There is a huge unmet need for autoantigen-specific therapy, without affecting the immune response against pathogens. This goal can be achieved by targeting autoantigen-specific T or B cells and by restoring self-tolerance by inducing tolerogenic antigen-presenting cells (APC) and the development of regulatory T (Treg) cells, for example, by using autoantigenic peptides bound to nanoparticles. Transferring in vitro manipulated autologous tolerogenic APC or autologous autoantigen-specific Treg cells to patients is the promising approach to develop cellular therapeutics. Most recently, chimeric autoantibody receptor T cells have been designed to specifically deplete autoreactive B cells. Limitations of these novel autoantigen-specific therapies will also be discussed.

Indexed as

AnimalsAutoantigensAutoimmune DiseasesAutoimmunityB-LymphocytesEncephalomyelitis, Autoimmune, ExperimentalHumansImmune ToleranceT-LymphocytesT-Lymphocytes, RegulatoryAutoantigensAntigen-specificAutoimmuneDiseasesNanoparticlesPeptidesTherapies

Identifiers

PMID34554499
OpenAlexW3127220371

What Socratic 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 Socratic graph.