ArticleNature microbiology2019
Evasion of autophagy mediated by Rickettsia surface protein OmpB is critical for virulence.
Article in Nature microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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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.
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.
Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Genomic evolution and adaptation of arthropod-associated Rickettsia.Scientific reports · 2022Pooled it
- Rickettsial Diseases and Vaccines: Is There an Opportunity for Plant-Made Vaccine Technology?Biotechnology and bioengineering · 2026Review
- Innate immune responses to Rickettsia: emerging themes and contrasts between species.Current opinion in microbiology · 2026Review
- DRP1/DMNL-1-mediated mitochondrial fission augmentsInfection and immunity · 2026Article
- Review
- Proximity labeling of thebioRxiv : the preprint server for biology · 2026Article
- Cryo-electron tomography reveals OmpB is required for themicroPublication biology · 2026Article
- Obligate intracellular bacteria and host cell death pathways-the matter of life and death.Cell and tissue research · 2025Review
- Deciphering macrophage dynamics and immune evasion strategies by the intracellular bacteria.Immunologic research · 2025Review
- Article
- ATG9 inhibitsAutophagy · 2025Article
- TlyC, a conserved hemolysin inMicrobiology spectrum · 2025Article
- Host glutathione is required for Rickettsia parkeri cell division and intracellular survival.Nature communications · 2025Article
- Differences between human and rodent nitric oxide production dictate susceptibility to tick-bornebioRxiv : the preprint server for biology · 2025Article
- Phosphatidylserine-binding receptor, CD300f, on macrophages mediates host invasion of pathogenic and non-pathogenic rickettsiae.Infection and immunity · 2025Article
- Polysaccharide synthesis operon modulates Rickettsia-endothelial cell interactions.PLoS pathogens · 2025Article
- HaloPROTAC3 does not trigger the degradation of the halotagged parasitophorous vacuole membrane protein UIS4 during Plasmodium liver stage development.Scientific reports · 2025Article
- Rickettsia parkeri forms extensive, stable contacts with the rough endoplasmic reticulum.The Journal of cell biology · 2025Article
- Development of a Recombinase-Mediated Cassette Exchange System for Gene Knockout and Expression of Non-Native Gene Sequences inVaccines · 2025Article
- The battle between bacterial infection and autophagy in aquatic animals.Frontiers in immunology · 2025Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Rickettsia are obligate intracellular bacteria that evade antimicrobial autophagy in the host cell cytosol by unknown mechanisms. Other cytosolic pathogens block different steps of autophagy targeting, including the initial step of polyubiquitin-coat formation. One mechanism of evasion is to mobilize actin to the bacterial surface. Here, we show that actin mobilization is insufficient to block autophagy recognition of the pathogen Rickettsia parkeri. Instead, R. parkeri employs outer membrane protein B (OmpB) to block ubiquitylation of the bacterial surface proteins, including OmpA, and subsequent recognition by autophagy receptors. OmpB is also required for the formation of a capsule-like layer. Although OmpB is dispensable for bacterial growth in endothelial cells, it is essential for R. parkeri to block autophagy in macrophages and to colonize mice because of its ability to promote autophagy evasion in immune cells. Our results indicate that OmpB acts as a protective shield to obstruct autophagy recognition, thereby revealing a distinctive bacterial mechanism to evade antimicrobial autophagy.
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Registered trials
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.