ArticleNature microbiology2018
Chlamydia trachomatis paralyses neutrophils to evade the host innate immune response.
Article in Nature microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed.
- An organotypic ectocervix mucosa model to study host-pathogen interaction of sexually transmitted infections.Materials today. Bio · 2026Article
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- Chlamydia trachomatis orchestrates multifaceted host cell manipulation for immune evasion.Communications biology · 2026Review
- ThemBio · 2026Article
- Reframing ME/CFS: toward a unified mechanistic model of chronic post-infectious diseases.Journal of translational medicine · 2026Review
- AFrontiers in immunology · 2026Article
- miRNA/mRNA analysis of increased TGF-β pathways drive epithelial-mesenchymal transition and regulatory T cell differentiation.Frontiers in immunology · 2026Article
- A single-tube RAA-CRISPR-Cas12a diagnostic platform for rapid detection of Chlamydia trachomatis.Journal of biological engineering · 2025Article
- Obligate intracellular bacteria and host cell death pathways-the matter of life and death.Cell and tissue research · 2025Review
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- Neutrophils at the Maternal-Fetal Interface: Agents of Protection or Destruction?American journal of reproductive immunology (New York, N.Y. : 1989) · 2025Review
- Biologic drug development for treatment and prevention of sexually transmitted infections.Clinical microbiology reviews · 2025Review
- miRNA/mRNA analysis of increased TGF-β pathways drive epithelial-mesenchymal transition and regulatory T cell differentiation.bioRxiv : the preprint server for biology · 2025Article
- Article
- A Cyclic-di-AMP Adjuvanted CPAF Protein Vaccine Is Immunogenic in Swine, but It Fails to Reduce GenitalVaccines · 2025Article
- Chlamydial protease-like activity factor targets SLC7A11 for degradation to induce ferroptosis and facilitate progeny releases.PLoS pathogens · 2025Article
- Low-Frequency, Sustained CD4 T-Cell Responses Chlamydia trachomatis in Women: Predominant Targeting of Chlamydial Proteaselike Activity Factor (CPAF).The Journal of infectious diseases · 2025Article
- Pathogenic and Protective Roles of Neutrophils inPathogens (Basel, Switzerland) · 2025Review
- Influence of cervicovaginal microbiota onMicrobial cell (Graz, Austria) · 2025Review
- Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chlamydia trachomatis, an obligate intracellular human pathogen, is a major cause of sexually transmitted diseases. Infections often occur without symptoms, a feature that has been attributed to the ability of the pathogen to evade the host immune response. We show here that C. trachomatis paralyses the host immune system by preventing the activation of polymorphic nuclear leukocytes (PMNs). PMNs infected with Chlamydia fail to produce neutrophil extracellular traps and the bacteria are able to survive in PMNs for extended periods of time. We have identified the secreted chlamydial protease-like activating factor (CPAF) as an effector mediating the evasion of the innate immune response since CPAF-deficient Chlamydia activate PMNs and are subsequently efficiently killed. CPAF suppresses the oxidative burst and interferes with chemical-mediated activation of neutrophils. We identified formyl peptide receptor 2 (FPR2) as a target of CPAF. FPR2 is cleaved by CPAF and released from the surface of PMNs. In contrast to previously described subversion mechanisms that mainly act on already activated PMNs, we describe here details of how Chlamydia actively paralyses PMNs, including the formation of neutrophil extracellular traps, to evade the host's innate immune response.
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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.