Evidence map›Paper›PMID 32591922›Full record

ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2020

Harnessing Newton's third-law paradigm to treat autoimmune diseases and chronic inflammations.

Tue Gia Nguyen

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 58% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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.

Tue Gia NguyenIgD Mab Technology (IMT) Group, Sydney, NSW, 2113, Australia. ceo-imt@igdmabtech.com.ORCID http://orcid.org/0000-0002-9685-7820
University of Technology Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeIt paradoxically seems counter-intuitive to consider treatments that activate the immune systems as a method to treat autoimmune diseases and chronic inflammations when these inflammatory conditions are themselves manifested by dysregulated activations of the immune responses. However, according to Newton's Third-Law of fundamental physics which formally states "For every action, there is an equal and opposite reaction", it can be reasonably argued that "For every activated pro-inflammatory response, there is an opposite and intrinsic anti-inflammatory response to follow." Therefore, harnessing these intrinsic self-regulated negative-feedbacks of anti-inflammatory and tolerogenic responses by activating the immune systems represents a novel therapeutic paradigm.

methodsThis review endeavoured to examine and discuss the current clinical and experimental evidences and therapeutic potentials of activating the innate and adaptive immune systems via their classical cell receptors, namely Toll-like receptors (TLRs), T-cell receptors (TCRs), and B cell receptors (BCRs), to modulate and suppress pathogenic inflammations.

resultsThe evidence presented in this review illustrated the therapeutic potentials and the caveats of  recent approaches and advances in harnessing this unorthodox therapeutic paradigm in the treatments of autoimmune diseases, allergic and chronic inflammations. It highlighted the promising potentials of targeting BCR-activated tolergenic responses as a new approach in this new therapeutic paradigm.

Indexed as

Adaptive ImmunityAnimalsAutoimmune DiseasesHomeostasisHumansImmune ToleranceImmunity, InnateImmunotherapyInflammationReceptors, Antigen, B-CellReceptors, Antigen, T-CellToll-Like Receptor 4Receptors, Antigen, B-CellReceptors, Antigen, T-CellToll-Like Receptor 4Adaptive immunityAllergyAutoimmune diseasesB cellsIgDImmune toleranceImmunomodulationImmunotherapyInflammationInnate immunity

Identifiers

PMID32591922
OpenAlexW3037933355

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.