Evidence map›Paper›PMID 38446856›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2024

How persistent infection overcomes peripheral tolerance mechanisms to cause T cell-mediated autoimmune disease.

Rose Yin, Samuel Melton, Eric S Huseby, Mehran Kardar, Arup K Chakraborty

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. 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

5 authors at 3 institutions in 1 country.

Rose Yin *Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139.
Samuel Melton *Physics of Living Systems, Department of Physics, Massachusetts Institute of Technology, Cambridge, MA 02139.
Eric S HusebyBasic Pathology, Department of Pathology, University of Massachusetts Medical School, Worcester, MA 01655.
Mehran KardarPhysics of Living Systems, Department of Physics, Massachusetts Institute of Technology, Cambridge, MA 02139.ORCID 0000-0002-1112-5912
Arup K ChakrabortyDepartment of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139.
Massachusetts Institute of Technology · USRagon Institute of MGH, MIT and Harvard · USUniversity of Massachusetts Chan Medical School · US

Funding

Origin and Control of Self-Reactive TCRsR01DK095077 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HUSEBY, ERIC S · 2012 to 2016
$1.8M
Massachusetts Institute of Technology (MIT) Physics of Living Systems FellowshipNational Science Foundation (NSF) 2141064National Science Foundation (NSF) DMR-2218849NIDDK NIH HHS R01 DK095077Ragon Institute of MGH, MIT and Harvard (Ragon Institute) 220568
6 · The paper itself

Abstract

T cells help orchestrate immune responses to pathogens, and their aberrant regulation can trigger autoimmunity. Recent studies highlight that a threshold number of T cells (a quorum) must be activated in a tissue to mount a functional immune response. These collective effects allow the T cell repertoire to respond to pathogens while suppressing autoimmunity due to circulating autoreactive T cells. Our computational studies show that increasing numbers of pathogenic peptides targeted by T cells during persistent or severe viral infections increase the probability of activating T cells that are weakly reactive to self-antigens (molecular mimicry). These T cells are easily re-activated by the self-antigens and contribute to exceeding the quorum threshold required to mount autoimmune responses. Rare peptides that activate many T cells are sampled more readily during severe/persistent infections than in acute infections, which amplifies these effects. Experiments in mice to test predictions from these mechanistic insights are suggested.

Indexed as

Autoimmune DiseasesPersistent InfectionAnimalsAutoantigensMicePeptidesPeripheral ToleranceT-LymphocytesAutoantigensPeptidesautoimmunityimmunologyT cells

Identifiers

PMID38446856
PMCPMC10945823
OpenAlexW4392502935

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.