ArticleAmerican journal of reproductive immunology (New York, N.Y. : 1989)2013
IL-23 induces IL-22 and IL-17 production in response to Chlamydia muridarum genital tract infection, but the absence of these cytokines does not influence disease pathogenesis.
Article in American journal of reproductive immunology (New York, N.Y. : 1989), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- CXCR6 marks polyfunctional effector CD4 T cells required for anti-bioRxiv : the preprint server for biology · 2026Article
- Chlamydia trachomatis orchestrates multifaceted host cell manipulation for immune evasion.Communications biology · 2026Review
- Endoplasmic reticulum: the target of chlamydial manipulation.Archives of microbiology · 2025Review
- Infectivity of a pathogenicity-attenuatedInfection and immunity · 2025Article
- Chlamydia muridarum Causes Persistent Subclinical Infection and Elicits Innate and Adaptive Immune Responses in C57BL/6J, BALB/cJ, and J:ARC(S) Mice Following Exposure to Shedding Mice.Comparative medicine · 2024Article
- Article
- IL-23 receptor signaling licenses group 3-like innate lymphoid cells to restrict a live-attenuated oral Chlamydia vaccine in the gut.Infection and immunity · 2023Article
- Th17/Treg Imbalance: Implications in Lung Inflammatory Diseases.International journal of molecular sciences · 2023Review
- Cytokine profiling of samples positive for Chlamydia trachomatis and Human papillomavirus.PloS one · 2023Article
- Role of IL-22 in homeostasis and diseases of the skin.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2022Review
- The Role of IL-17 During Infections in the Female Reproductive Tract.Frontiers in immunology · 2022Review
- The hormonal environment and estrogen receptor signaling altersFrontiers in cellular and infection microbiology · 2022Article
- Pelvic Inflammatory Disease Due to Neisseria gonorrhoeae and Chlamydia trachomatis: Immune Evasion Mechanisms and Pathogenic Disease Pathways.The Journal of infectious diseases · 2021Review
- Ambroxol Treatment Suppresses the Proliferation ofMicroorganisms · 2021Article
- Microbiota-Dependent Effects of IL-22.Cells · 2020Review
- Inferring Regulatory Networks From Mixed Observational Data Using Directed Acyclic Graphs.Frontiers in genetics · 2020Article
- Parenteral vaccination protects against transcervical infection withNPJ vaccines · 2020Article
- The Immunoregulation of Th17 in Host against Intracellular Bacterial Infection.Mediators of inflammation · 2018Review
- Immunofibrogenic Gene Expression Patterns in Tanzanian Children with OcularFrontiers in cellular and infection microbiology · 2017Article
- IFNγ is Required for Optimal Antibody-Mediated Immunity against Genital Chlamydia Infection.Infection and immunity · 2016Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
objectiveChlamydia trachomatis infections are a significant cause of reproductive tract pathology. Protective and pathological immune mediators must be differentiated to design a safe and effective vaccine.
methodsWild-type mice and mice deficient in IL-22 and IL-23 were infected intravaginally with Chlamydia muridarum, and their course of infection and oviduct pathology were compared. Local genital tract and draining lymph node immune responses were also examined in IL-23-deficient mice.
resultsIL-22- and IL-23-deficient mice exhibited normal susceptibility to infection and oviduct pathology. IL-23 was required for the development of a Chlamydia-specific Th17 response in the lymph nodes and for production of IL-22 and IL-17 in the genital tract. However, influx of Th1 and innate immune cells was not compromised in the absence of IL-23.
conclusionIL-22 and IL-23 play either redundant or minimal roles in the pathogenesis of Chlamydia infection in the mouse model. Induction of Th17-associated cytokines by a Chlamydia vaccine should be avoided as these responses are not central to resolution of infection and have pathologic potential.
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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.