ArticleMucosal immunology2015
Immune requirements for protective Th17 recall responses to Mycobacterium tuberculosis challenge.
Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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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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
57 citing papers in PubMed, 97 citations in OpenAlex.
- Context-specific roles for IL-17 in tuberculosis.PLoS pathogens · 2026Review
- Sex as a Biological Variable in Tuberculosis Pathogenesis.Immunological reviews · 2026Review
- HIV impairs and exploits pulmonary Th17 and Th22 cell-mediated immune responses to Mycobacterium tuberculosis.PLoS pathogens · 2026Article
- Novel Multistage SubunitVaccines · 2025Article
- IFN-γ and IL-17 elicit synergistic anti-mycobacterial responses by inhibiting coronin-1A retention.Communications biology · 2025Article
- Mincle receptor agonist UM-1098 and TLR4 agonist INI-2002 combination adjuvant enhances Th1 responses and provides protection againstVaccine: X · 2025Article
- Using host and bacterial genetic approaches to define virulence strategies and protective immunity duringmSphere · 2025Review
- Article
- Uncovering the Bronchoalveolar Single-Cell Landscape of Patients With Pulmonary Tuberculosis With Human Immunodeficiency Virus Type 1 Coinfection.The Journal of infectious diseases · 2024Article
- Vaccination with Mincle agonist UM-1098 and mycobacterial antigens induces protective Th1 and Th17 responses.NPJ vaccines · 2024Article
- A protective role for type I interferon signaling following infection with Mycobacterium tuberculosis carrying the rifampicin drug resistance-conferring RpoB mutation H445Y.PLoS pathogens · 2024Article
- The role of the immune response in developing tuberculosis infection: from latent infection to active tuberculosis.Frontiers in tuberculosis · 2024Review
- A Key Role of CD8+ T Cells in Controlling of Tuberculosis Infection.Diagnostics (Basel, Switzerland) · 2023Article
- Tuberculosis and COVID-19 Dually Affect Human Th17 Cell Immune Response.Biomedicines · 2023Review
- Article
- Bridging the gaps to overcome major hurdles in the development of next-generation tuberculosis vaccines.Frontiers in immunology · 2023Review
- Molecular and Cellular Mechanisms ofInternational journal of molecular sciences · 2022Review
- Mucosal Vaccination with Cyclic Dinucleotide Adjuvants Induces Effective T Cell Homing and IL-17-Dependent Protection againstJournal of immunology (Baltimore, Md. : 1950) · 2022Article
- It Takes a Village: The Multifaceted Immune Response toFrontiers in immunology · 2022Review
- The protective role of tissue-resident interleukin 17A-producing gamma delta T cells in MycobacteriumFrontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Tuberculosis (TB) vaccine development has focused largely on targeting T helper type 1 (Th1) cells. However, despite inducing Th1 cells, the recombinant TB vaccine MVA85A failed to enhance protection against TB disease in humans. In recent years, Th17 cells have emerged as key players in vaccine-induced protection against TB. However, the exact cytokine and immune requirements that enable Th17-induced recall protection remain unclear. In this study, we have investigated the requirements for Th17 cell-induced recall protection against Mycobacterium tuberculosis (Mtb) challenge by utilizing a tractable adoptive transfer model in mice. We demonstrate that adoptive transfer of Mtb-specific Th17 cells into naive hosts, and upon Mtb challenge, results in Th17 recall responses that confer protection at levels similar to vaccination strategies. Importantly, although interleukin (IL)-23 is critical, IL-12 and IL-21 are dispensable for protective Th17 recall responses. Unexpectedly, we demonstrate that interferon-γ (IFN-γ) produced by adoptively transferred Th17 cells impairs long-lasting protective recall immunity against Mtb challenge. In contrast, CXCR5 expression is crucial for localization of Th17 cells near macrophages within well-formed B-cell follicles to mediate Mtb control. Thus, our data identify new immune characteristics that can be harnessed to improve Th17 recall responses for enhancing vaccine design against TB.
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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.