ArticlePloS one2012
Neisseria gonorrhoeae suppresses dendritic cell-induced, antigen-dependent CD4 T cell proliferation.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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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
37 citing papers in PubMed, 56 citations in OpenAlex.
- Mechanisms, management and prevention of anorectal sexually transmitted infections.Nature reviews. Gastroenterology & hepatology · 2026Review
- Walking the tightrope: Balancing immune checkpoints and their inhibitors in host defence against bacterial infections.Journal of applied biomedicine · 2026Review
- Beyond Inflammation: A Comprehensive Outlook on the Integrated Traditional Chinese and Western Medicine Treatment of Pelvic Inflammatory Disease.International journal of general medicine · 2026Review
- Terminal complement complexes with or without C9 potentiate antimicrobial activity againstmBio · 2025Article
- Neisseria gonorrhoeae induces local secretion of IL-10 at the human cervix to promote colonization.The Journal of clinical investigation · 2024Article
- Gonococcal PorB: a multifaceted modulator of host immune responses.Trends in microbiology · 2024Review
- Gonococcal microparticle vaccine in dissolving microneedles induced immunity and enhanced bacterial clearance in infected mice.International journal of pharmaceutics · 2023Article
- Article
- Commensal Neisseria species share immune suppressive mechanisms with Neisseria gonorrhoeae.PloS one · 2023Article
- Mechanisms of host manipulation byFrontiers in microbiology · 2023Review
- Fascinating Molecular and Immune Escape Mechanisms in the Treatment of STIs (Syphilis, Gonorrhea, Chlamydia, and Herpes Simplex).International journal of molecular sciences · 2022Review
- Systemic and Mucosal Concentrations of Nine Cytokines Among Individuals withAAS open research · 2022Article
- Tissue Models forFrontiers in cellular and infection microbiology · 2022Review
- Pelvic Inflammatory Disease Due to Neisseria gonorrhoeae and Chlamydia trachomatis: Immune Evasion Mechanisms and Pathogenic Disease Pathways.The Journal of infectious diseases · 2021Review
- Vaccine Candidates for the Control and Prevention of the Sexually Transmitted Disease Gonorrhea.Vaccines · 2021Review
- Review
- Potential of Mesenchymal Stem Cell-Derived Exosomes as a Novel Treatment for Female Infertility Caused by Bacterial Infections.Frontiers in microbiology · 2021Review
- The serogroup B meningococcal outer membrane vesicle-based vaccine 4CMenB induces cross-species protection against Neisseria gonorrhoeae.PLoS pathogens · 2020Article
- Novel Whole-Cell InactivatedVaccines · 2018Article
- Properly folded and functional PorB fromThe Journal of biological chemistry · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Neisseria gonorrhoeae is the second most common sexually transmitted bacterial pathogen worldwide. Diseases associated with N. gonorrhoeae cause localized inflammation of the urethra and cervix. Despite this inflammatory response, infected individuals do not develop protective adaptive immune responses to N. gonorrhoeae. N. gonorrhoeae is a highly adapted pathogen that has acquired multiple mechanisms to evade its host's immune system, including the ability to manipulate multiple immune signaling pathways. N. gonorrhoeae has previously been shown to engage immunosuppressive signaling pathways in B and T lymphocytes. We have now found that N. gonorrhoeae also suppresses adaptive immune responses through effects on antigen presenting cells. Using primary, murine bone marrow-derived dendritic cells and lymphocytes, we show that N. gonorrhoeae-exposed dendritic cells fail to elicit antigen-induced CD4+ T lymphocyte proliferation. N. gonorrhoeae exposure leads to upregulation of a number of secreted and dendritic cell surface proteins with immunosuppressive properties, particularly Interleukin 10 (IL-10) and Programmed Death Ligand 1 (PD-L1). We also show that N. gonorrhoeae is able to inhibit dendritic cell- induced proliferation of human T-cells and that human dendritic cells upregulate similar immunosuppressive molecules. Our data suggest that, in addition to being able to directly influence host lymphocytes, N. gonorrhoeae also suppresses development of adaptive immune responses through interactions with host antigen presenting cells. These findings suggest that gonococcal factors involved in host immune suppression may be useful targets in developing vaccines that induce protective adaptive immune responses to this pathogen.
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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.