Evidence map›Paper›PMID 38380317›Full record

ReviewFrontiers in immunology2024

Mechanisms underlying immunosuppression by regulatory cells.

Oliver Goldmann, Obiageli Vivian Nwofor, Qian Chen, Eva Medina

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 3 pooled it
25.3field-weighted citation impact, top 1% 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

101 citing papers in PubMed, 3 syntheses or guidelines pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Dynamic regulation of CD300b and CD300f on myeloid cells in oral immunotherapy.The journal of allergy and clinical immunology. Global · 2026
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  9. The TPx Protein ofCells · 2026
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  13. Anti-Inflammatory Potential ofMicroorganisms · 2026
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  20. Article

41 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Oliver GoldmannInfection Immunology Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Obiageli Vivian NwoforInfection Immunology Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Qian ChenInfection Immunology Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Eva MedinaInfection Immunology Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Helmholtz Centre for Infection Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulatory cells, such as regulatory T cells (Tregs), regulatory B cells (Bregs), and myeloid-derived suppressor cells (MDSCs), play a crucial role in preserving immune tolerance and controlling immune responses during infections to prevent excessive immune activation. However, pathogens have developed strategies to hijack these regulatory cells to decrease the overall effectiveness of the immune response and persist within the host. Consequently, therapeutic targeting of these immunosuppressive mechanisms during infection can reinvigorate the immune response and improve the infection outcome. The suppressive mechanisms of regulatory cells are not only numerous but also redundant, reflecting the complexity of the regulatory network in modulating the immune responses. The context of the immune response, such as the type of pathogen or tissue involved, further influences the regulatory mechanisms involved. Examples of these immunosuppressive mechanisms include the production of inhibitory cytokines such as interleukin 10 (IL-10) and transforming growth factor beta (TGF-β) that inhibit the production of pro-inflammatory cytokines and dampen the activation and proliferation of effector T cells. In addition, regulatory cells utilize inhibitory receptors like cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) to engage with their respective effector cells, thereby suppressing their function. An alternative approach involves the modulation of metabolic reprogramming in effector immune cells to limit their activation and proliferation. In this review, we provide an overview of the major mechanisms mediating the immunosuppressive effect of the different regulatory cell subsets in the context of infection.

Indexed as

Immune ToleranceT-Lymphocytes, RegulatoryCytokinesImmunosuppression TherapyTransforming Growth Factor betaCytokinesTransforming Growth Factor betaimmunosuppressive mechanismsinfectionmyeloid-derived suppressor cellsregulatory B cellsregulatory T cells

Identifiers

PMID38380317
PMCPMC10876998
OpenAlexW4391573779

What OpenQuestion 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 OpenQuestion graph.