Evidence map›Paper›PMID 35396464›Full record

ReviewNature reviews. Immunology2022

Bacterial origins of human cell-autonomous innate immune mechanisms.

Tanita Wein, Rotem Sorek

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers.

0numbers the graph read from it
0cells of the map it votes in
138citing papers in PubMed
–field-weighted citation impact
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

138 citing papers in PubMed.

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  16. The heat-ramp method to study regulated cell death in a pathogenic yeastbioRxiv : the preprint server for biology · 2026
    Article
  17. Review
  18. cGAS-STING signaling pathway in MASLD and liver fibrosis.Journal of molecular medicine (Berlin, Germany) · 2026
    Review
  19. Review
  20. Review

78 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

2 authors.

Tanita WeinDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
Rotem SorekDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel. rotem.sorek@weizmann.ac.il.ORCID 0000-0002-3872-4982

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cell-autonomous innate immune system enables animal cells to resist viral infection. This system comprises an array of sensors that, after detecting viral molecules, activate the expression of antiviral proteins and the interferon response. The repertoire of immune sensors and antiviral proteins has long been considered to be derived from extensive evolutionary innovation in vertebrates, but new data challenge this dogma. Recent studies show that central components of the cell-autonomous innate immune system have ancient evolutionary roots in prokaryotic genes that protect bacteria from phages. These include the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway, Toll/IL-1 receptor (TIR) domain-containing pathogen receptors, the viperin family of antiviral proteins, SAMHD1-like nucleotide-depletion enzymes, gasdermin proteins and key components of the RNA interference pathway. This Perspective details current knowledge of the elements of antiviral immunity that are conserved from bacteria to humans, and presents possible evolutionary scenarios to explain the observed conservation.

Indexed as

NucleotidyltransferasesSignal TransductionAnimalsBacteriaHumansImmunity, InnateInterferonsNucleotidesReceptors, Interleukin-1SAM Domain and HD Domain-Containing Protein 1InterferonsNucleotidesNucleotidyltransferasesReceptors, Interleukin-1SAM Domain and HD Domain-Containing Protein 1

Identifiers

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.