ArticlePLoS pathogens2022
Th1 cells are dispensable for primary clearance of Chlamydia from the female reproductive tract of mice.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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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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.
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Who cites it
18 citing papers in PubMed, 19 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
- Immunization with a multisubunit vaccine induces immunological memory and cross-protective immunity against heterologousFrontiers in cellular and infection microbiology · 2026Article
- AFrontiers in immunology · 2026Article
- Post-exposure vaccine protection of CTH522/CAFNPJ vaccines · 2025Article
- T cell signatures associated with reduced Chlamydia trachomatis reinfection in a highly exposed cohort.JCI insight · 2025Article
- A VCG-Based MultiepitopeBiomedicines · 2025Article
- Irradiated whole cell Chlamydia vaccine confers significant protection in a murine genital tract challenge model.NPJ vaccines · 2024Article
- Immunity to Sexually Transmitted Bacterial Infections of the Female Genital Tract: Toward Effective Vaccines.Vaccines · 2024Review
- Elimination of Chlamydia muridarum from the female reproductive tract is IL-12p40 dependent, but independent of Th1 and Th2 cells.PLoS pathogens · 2024Article
- Koala ocular disease grades are defined by chlamydial load changes and increases in Th2 immune responses.Frontiers in cellular and infection microbiology · 2024Article
- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against Chlamydia.PLoS pathogens · 2024Article
- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract againstbioRxiv : the preprint server for biology · 2023Article
- Optimal generation of hepatic tissue-resident memory CD4 T cells requires IL-1 and IL-2.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Regulation of chlamydial colonization by IFNγ delivered via distinct cells.Trends in microbiology · 2023Review
- IFNγ and Antibody Synergize To Enhance Protective Immunity against Chlamydia Dissemination and Female Reproductive Tract Reinfections.Infection and immunity · 2022Article
- Efficacy of Pgp3 vaccination forFrontiers in immunology · 2022Article
- (Not) Home alone: Antigen presenting cell - T Cell communication in barrier tissues.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Protective immune responses to Chlamydia infection within the female reproductive tract (FRT) are incompletely understood. MHC class II-restricted CD4 Th1 responses are believed to be vital for bacterial clearance due to their capacity to secrete IFN-γ, but an essential requirement for T-bet-expressing Th1 cells has yet to be demonstrated in the mouse model of Chlamydia infection. Here, we investigated the role of T-bet and IFN-γ in primary clearance of Chlamydia after FRT infection. Surprisingly, IFN-γ producing CD4 T cells from the FRT expressed low levels of T-bet throughout infection, suggesting that classical T-bet-expressing Th1 cells are inefficiently generated and therefore unlikely to participate in bacteria clearance. Furthermore, mice deficient in T-bet expression or with a CD4-specific T-bet deficiency cleared FRT infection similarly to wild-type controls. T-bet-deficient mice displayed significant skewing of FRT CD4 T cells towards Th17 responses, demonstrating that compensatory effector pathways are generated in the absence of Th1 cells. In marked contrast, IFN-γ-, and IFN-γR-deficient mice were able to reduce FRT bacterial burdens, but suffered systemic bacterial dissemination and 100% mortality. Together, these data demonstrate that IFN-γ signaling is essential to protect mice from fatal systemic disease, but that classical T-bet-expressing Th1 cells are non-essential for primary clearance within the FRT. Exploring the protective contribution of Th1 cells versus other CD4 effector lineages could provide important information for the generation of new Chlamydia vaccines.
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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.