ArticlePLoS pathogens2015
EphrinA2 receptor (EphA2) is an invasion and intracellular signaling receptor for Chlamydia trachomatis.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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.
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
76 citing papers in PubMed, 109 citations in OpenAlex.
- Sphingolipids associate with the chlamydial nucleoid and mark developmental transitions in Chlamydia trachomatis.Nature communications · 2026Article
- An organotypic ectocervix mucosa model to study host-pathogen interaction of sexually transmitted infections.Materials today. Bio · 2026Article
- Chlamydia trachomatis orchestrates multifaceted host cell manipulation for immune evasion.Communications biology · 2026Review
- Emerging host-directed strategies for overcoming drug resistance and immune evasion in Staphylococcus aureus infections.Journal of advanced research · 2026Review
- METTL14-Mediated Inhibition of Apoptosis via the MAPK and PI3K/AKT Pathways PromotesMicroorganisms · 2026Article
- PTEN Loss Promotes PI3Kβ Phosphorylation and EPHA2/SRC/p-PI3KβY962 Complex Assembly to Drive Tumorigenesis.Cancer discovery · 2026Article
- Review
- Pathogenicity and virulence ofVirulence · 2025Review
- Dcaf15-mediated EphA2 degradation triggers disruption of the blood-brain barrier during Streptococcus suis meningitis.Communications biology · 2025Article
- Chlamydia trachomatis invasion: a duet of effectors.Biochemical Society transactions · 2025Review
- Dectin-1 stimulating β-glucans inhibit Chlamydia infections both in vitro and in vivo.Pathogens and disease · 2025Article
- Irradiated whole cell Chlamydia vaccine confers significant protection in a murine genital tract challenge model.NPJ vaccines · 2024Article
- Infection of human organoids supports an intestinal niche for Chlamydia trachomatis.PLoS pathogens · 2024Article
- Insights into Chlamydia Development and Host Cells Response.Microorganisms · 2024Review
- Chlamydia trachomatis enhances HPV persistence through immune modulation.BMC infectious diseases · 2024Article
- Claudin-1 interacts with EPHA2 to promote cancer stemness and chemoresistance in colorectal cancer.Cancer letters · 2023Article
- Intracellular lifestyle of Chlamydia trachomatis and host-pathogen interactions.Nature reviews. Microbiology · 2023Review
- Out of the ESCPE room: Emerging roles of endosomal SNX-BARs in receptor transport and host-pathogen interaction.Traffic (Copenhagen, Denmark) · 2023Review
- Review
- Establishing the intracellular niche of obligate intracellular vacuolar pathogens.Frontiers in cellular and infection microbiology · 2023Review
16 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
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The obligate intracellular bacterium Chlamydia trachomatis invades into host cells to replicate inside a membrane-bound vacuole called inclusion. Multiple different host proteins are recruited to the inclusion and are functionally modulated to support chlamydial development. Invaded and replicating Chlamydia induces a long-lasting activation of the PI3 kinase signaling pathway that is required for efficient replication. We identified the cell surface tyrosine kinase EphrinA2 receptor (EphA2) as a chlamydial adherence and invasion receptor that induces PI3 kinase (PI3K) activation, promoting chlamydial replication. Interfering with binding of C. trachomatis serovar L2 (Ctr) to EphA2, downregulation of EphA2 expression or inhibition of EphA2 activity significantly reduced Ctr infection. Ctr interacts with and activates EphA2 on the cell surface resulting in Ctr and receptor internalization. During chlamydial replication, EphA2 remains active accumulating around the inclusion and interacts with the p85 regulatory subunit of PI3K to support the activation of the PI3K/Akt signaling pathway that is required for normal chlamydial development. Overexpression of full length EphA2, but not the mutant form lacking the intracellular cytoplasmic domain, enhanced PI3K activation and Ctr infection. Despite the depletion of EphA2 from the cell surface, Ctr infection induces upregulation of EphA2 through the activation of the ERK pathway, which keeps the infected cell in an apoptosis-resistant state. The significance of EphA2 as an entry and intracellular signaling receptor was also observed with the urogenital C. trachomatis-serovar D. Our findings provide the first evidence for a host cell surface receptor that is exploited for invasion as well as for receptor-mediated intracellular signaling to facilitate chlamydial replication. In addition, the engagement of a cell surface receptor at the inclusion membrane is a new mechanism by which Chlamydia subverts the host cell and induces apoptosis resistance.
Indexed as
Identifiers
What OpenQuestion holds
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.