ArticleThe Journal of infectious diseases2018
Interleukin-21 Regulates Natural Killer Cell Responses During Mycobacterium tuberculosis Infection.
Article in The Journal of infectious diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
25 citing papers in PubMed, 42 citations in OpenAlex.
- Modulation of pulmonary IL-21 expression during latent TB and M. tuberculosis/SIV coinfection.JCI insight · 2026Article
- IFN-γ- GranzymeB + Natural killer cells are induced by IV BCG vaccination and associated with protection against tuberculosis in rhesus macaques.Mucosal immunology · 2026Article
- Cell-mediated immune responses of beta-glucan on the pathogenesis of chronic tuberculosis infection.Frontiers in immunology · 2026Review
- Cytotoxic granules and effector molecules from immune cells in tuberculosis: Mechanisms of host defense and therapeutic potential.Virulence · 2025Review
- B cells inhibit IL-1 family cytokine production and Mycobacterium tuberculosis growth in human CD14+ cells.ImmunoHorizons · 2025Article
- IL-21-dependent Ly6CCell death discovery · 2025Article
- Diverse potential of chimeric antigen receptor-engineered cell therapy: Beyond cancer.Clinical and translational medicine · 2025Review
- COMPREHENSIVE CHARACTERIZATION OF CYTOKINES IN PATIENTS UNDER EXTRACORPOREAL MEMBRANE OXYGENATION: EVIDENCE FROM INTEGRATED BULK AND SINGLE-CELL RNA SEQUENCING DATA USING MULTIPLE MACHINE LEARNING APPROACHES.Shock (Augusta, Ga.) · 2025Article
- The Importance of Lung Innate Immunity During Health and Disease.Pathogens (Basel, Switzerland) · 2025Review
- Host Immune Response toJournal of inflammation research · 2025Review
- Granzyme B-producing B cells: a bidirectional relationship with breast cancer cells and implications for immunotherapy.American journal of clinical and experimental immunology · 2025Article
- Pro-inflammatory cytokine IL-21 correlates with the reactive oxygen species and 25-hydroxy vitamin D in rheumatoid arthritis patients.Immunity, inflammation and disease · 2024Article
- Clinical manifestations and immune response to tuberculosis.World journal of microbiology & biotechnology · 2023Review
- HIV-Differentiated Metabolite N-Acetyl-L-Alanine Dysregulates Human Natural Killer Cell Responses toInternational journal of molecular sciences · 2023Article
- Deciphering the virulence factors, regulation, and immune response toFrontiers in cellular and infection microbiology · 2023Review
- Leveraging Natural Killer Cell Innate Immunity against Hematologic Malignancies: From Stem Cell Transplant to Adoptive Transfer and Beyond.International journal of molecular sciences · 2022Review
- Costimulatory CD226 Signaling Regulates Proliferation of Memory-like NK Cells in Healthy Individuals with LatentInternational journal of molecular sciences · 2022Article
- Evaluation of early innate and adaptive immune responses to the TB vaccine Mycobacterium bovis BCG and vaccine candidate BCGΔBCG1419c.Scientific reports · 2022Article
- IL-21/IL-21R Regulates the Neutrophil-Mediated Pathologic Immune Response during Chlamydial Respiratory Infection.Mediators of inflammation · 2022Article
- Exploiting Pre-Existing CD4Journal of immunology (Baltimore, Md. : 1950) · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Background: In the current study, we determined the effects of interleukin (IL)-21 on human natural killer (NK) cells and monocyte responses during Mycobacterium tuberculosis (Mtb) infection. Methods: We found that Mtb stimulated CD4+ and NK T cells from healthy individuals with latent tuberculosis infection (LTBI+) are major sources of IL-21. CD4+ cells from tuberculosis patients secreted less IL-21 than did CD4+ cells from healthy LTBI+ individuals. Interleukin-21 had no direct effect on Mtb-stimulated monocytes. Results: Interleukin-21-activated NK cells produced interferon (IFN)-γ, perforin, granzyme B, and granulysin; lysed Mtb-infected monocytes; and reduced Mtb growth. Interleukin-21-activated NK cells also enhanced IL-1β, IL-18, and CCL4/macrophage-inflammatory protein (MIP)-1β production and reduced IL-10 production by Mtb-stimulated monocytes. Recombinant IL-21 (1) inhibited Mtb growth, (2) enhanced IFN-γ, IL-1β, IL-18, and MIP-1β, and (3) reduced IL-10 expression in the lungs of Mtb-infected Rag2 knockout mice. Conclusions: These findings suggest that activated T cells enhance NK cell responses to lyse Mtb-infected human monocytes and restrict Mtb growth in monocytes through IL-21 production. Interleukin-21-activated NK cells also enhance the immune response by augmenting IL-1β, IL-18, and MIP-1β production and reducing IL-10 production by monocytes in response to an intracellular pathogen.
Indexed as
Identifiers
What OpenQuestion holds
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.