Evidence map›Paper›PMID 37626865›Full record

ArticleCells2023

Unraveling the Role of Toll-like Receptors in the Immunopathogenesis of Selected Primary and Secondary Immunodeficiencies.

Paulina Mertowska, Konrad Smolak, Sebastian Mertowski, Ewelina Grywalska

Open access · goldAbstract read
In one paragraph

Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. 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

4 authors at 1 institution in 1 country.

Paulina MertowskaDepartment of Experimental Immunology, Medical University of Lublin, 20-093 Lublin, Poland.ORCID 0000-0001-9530-6659
Konrad SmolakDepartment of Experimental Immunology, Medical University of Lublin, 20-093 Lublin, Poland.
Sebastian MertowskiDepartment of Experimental Immunology, Medical University of Lublin, 20-093 Lublin, Poland.ORCID 0000-0002-7121-1396
Ewelina GrywalskaDepartment of Experimental Immunology, Medical University of Lublin, 20-093 Lublin, Poland.ORCID 0000-0002-0451-4741
Medical University of Lublin · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human immune system is a complex network of cells, tissues, and molecules that work together to defend the body against pathogens and maintain overall health. However, in some individuals, the immune system fails to function correctly, leading to immunodeficiencies. Immunodeficiencies can be classified into primary (PID) and secondary (SID) types, each with distinct underlying causes and manifestations. Toll-like receptors (TLRs), as key components of the immune system, have been implicated in the pathogenesis of both PID and SID. In this study, we aim to unravel the intricate involvement of TLR2, TLR4, TLR3, TLR7, TLR8, and TLR9 in the immunopathogenesis of common variable immunodeficiency-CVID (as PID)-and chronic lymphocytic leukemia-CLL (as SID). The obtained results indicate a significant increase in the percentage of all tested subpopulations of T lymphocytes and B lymphocytes showing positive expression of all analyzed TLRs in patients with CVID and CLL compared to healthy volunteers, constituting the control group, which is also confirmed by analysis of the concentration of soluble forms of these receptors in the plasma of patients. Furthermore, patients diagnosed with CVID are characterized by the percentage of all lymphocytes showing positive expression of the tested TLR2, TLR4, TLR3, and TLR9 and their plasma concentrations in relation to patients with CLL. By investigating the functions and interactions of TLRs within the immune system, we seek to shed light on their critical role in the development and progression of these immunodeficiencies. Through a comprehensive analysis of the literature and presented experimental data, we hope to deepen our understanding of the complex mechanisms by which TLRs contribute to the pathogenesis of PID and SID. Ultimately, our findings may provide valuable insights into developing targeted therapeutic strategies to mitigate the impact of these disorders on those affected by immunodeficiency.

Indexed as

Common Variable ImmunodeficiencyImmunologic Deficiency SyndromesLeukemia, Lymphocytic, Chronic, B-CellHumansToll-Like Receptor 2Toll-Like Receptor 3Toll-Like Receptor 4Toll-Like Receptor 9Toll-Like Receptor 2Toll-Like Receptor 3Toll-Like Receptor 4Toll-Like Receptor 9CLLCVIDimmunodeficiencyPIDSIDTLR

Identifiers

PMID37626865
PMCPMC10453926
OpenAlexW4385811281

What OpenQuestion holds

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LicenceCC BY
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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.