Evidence map›Paper›PMID 36221902›Full record

ArticleThe EMBO journal2022

Selective autophagy of RIPosomes maintains innate immune homeostasis during bacterial infection.

Subhash Mehto, Kautilya Kumar Jena, Rina Yadav, Swatismita Priyadarsini, Pallavi Samal, Sivaram Krishna, Kollori Dhar, Ashish Jain, Nishant Ranjan Chauhan, Krushna C Murmu and 10 more

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Regulation of Innate Immune Signaling by Autophagy.International journal of molecular sciences · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. HEATR3 recognizes membrane rupture and facilitates xenophagy in response toProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Article
  10. Autophagy and Bacterial infections.Autophagy reports · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
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

20 authors at 6 institutions in 3 countries.

Subhash Mehto *Cell Biology and Infectious Diseases Unit, Department of Infectious Disease Biology, Institute of Life Sciences, Bhubaneswar, India.ORCID 0000-0002-5351-7850
Kautilya Kumar Jena *Cell Biology and Infectious Diseases Unit, Department of Infectious Disease Biology, Institute of Life Sciences, Bhubaneswar, India.ORCID 0000-0002-7568-1555
Rina YadavCell Biology and Infectious Diseases Unit, Department of Infectious Disease Biology, Institute of Life Sciences, Bhubaneswar, India.
Swatismita PriyadarsiniInstitute of Life Sciences, Bhubaneswar, India.
Pallavi SamalCell Biology and Infectious Diseases Unit, Department of Infectious Disease Biology, Institute of Life Sciences, Bhubaneswar, India.
Sivaram KrishnaCell Biology and Infectious Diseases Unit, Department of Infectious Disease Biology, Institute of Life Sciences, Bhubaneswar, India.ORCID 0000-0002-5287-8152
Kollori DharCell Biology and Infectious Diseases Unit, Department of Infectious Disease Biology, Institute of Life Sciences, Bhubaneswar, India.
Ashish JainCentre for Cancer Cell Reprogramming, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.ORCID 0000-0001-6549-2788
Nishant Ranjan ChauhanCell Biology and Infectious Diseases Unit, Department of Infectious Disease Biology, Institute of Life Sciences, Bhubaneswar, India.ORCID 0000-0002-9137-6024
Krushna C MurmuEpigenetic and Chromatin Biology Unit, Institute of Life Sciences, Bhubaneswar, India.ORCID 0000-0002-5568-680X
Ramyasingh BalCell Biology and Infectious Diseases Unit, Department of Infectious Disease Biology, Institute of Life Sciences, Bhubaneswar, India.
Rinku SahuCell Biology and Infectious Diseases Unit, Department of Infectious Disease Biology, Institute of Life Sciences, Bhubaneswar, India.ORCID 0000-0003-2990-0152
Pundrik JaiswalCell Biology and Infectious Diseases Unit, Department of Infectious Disease Biology, Institute of Life Sciences, Bhubaneswar, India.
Bhabani Sankar SahooInstitute of Life Sciences, Bhubaneswar, India.
Srinivas PatnaikSchool of Biotechnology, KIIT University, Bhubaneswar, India.
Thomas A KuferDepartment of Immunology, Institute of Nutritional Medicine, University of Hohenheim, Stuttgart, Germany.ORCID 0000-0003-4563-0412
Tor Erik RustenCentre for Cancer Cell Reprogramming, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.ORCID 0000-0002-9150-2676
Swati ChauhanEpigenetic and Chromatin Biology Unit, Institute of Life Sciences, Bhubaneswar, India.
Punit PrasadEpigenetic and Chromatin Biology Unit, Institute of Life Sciences, Bhubaneswar, India.
Santosh ChauhanCell Biology and Infectious Diseases Unit, Department of Infectious Disease Biology, Institute of Life Sciences, Bhubaneswar, India.ORCID 0000-0001-9167-5107
Institute of Life Sciences · INRegional Centre for Biotechnology · INCentre for Cellular and Molecular Biology · INOslo University Hospital · NOKIIT University · INUniversity of Hohenheim · DE

Funding

Wellcome Trust
6 · The paper itself

Abstract

The NOD1/2-RIPK2 is a key cytosolic signaling complex that activates NF-κB pro-inflammatory response against invading pathogens. However, uncontrolled NF-κB signaling can cause tissue damage leading to chronic diseases. The mechanisms by which the NODs-RIPK2-NF-κB innate immune axis is activated and resolved remain poorly understood. Here, we demonstrate that bacterial infection induces the formation of endogenous RIPK2 oligomers (RIPosomes) that are self-assembling entities that coat the bacteria to induce NF-κB response. Next, we show that autophagy proteins IRGM and p62/SQSTM1 physically interact with NOD1/2, RIPK2 and RIPosomes to promote their selective autophagy and limit NF-κB activation. IRGM suppresses RIPK2-dependent pro-inflammatory programs induced by Shigella and Salmonella. Consistently, the therapeutic inhibition of RIPK2 ameliorates Shigella infection- and DSS-induced gut inflammation in Irgm1 KO mice. This study identifies a unique mechanism where the innate immune proteins and autophagy machinery are recruited together to the bacteria for defense as well as for maintaining immune homeostasis.

Indexed as

Bacterial InfectionsNF-kappa BAnimalsAutophagyHomeostasisImmunity, InnateMiceMice, Inbred NODNF-kappa BautophagyinflammationIrgm1NOD1/2-RIPK2-NF-κBRIPosomes

Identifiers

PMID36221902
PMCPMC9713718
OpenAlexW4304631876

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.