ArticlePLoS pathogens2015
A rho GDP dissociation inhibitor produced by apoptotic T-cells inhibits growth of Mycobacterium tuberculosis.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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
12 citing papers in PubMed, 15 citations in OpenAlex.
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- Metabolic changes enhance necroptosis of type 2 diabetes mellitus mice infected with Mycobacterium tuberculosis.PLoS pathogens · 2024Article
- Role of ROCK signaling in virus replication.Virus research · 2023Review
- BCG vaccination reduces the mortality of Mycobacterium tuberculosis-infected type 2 diabetes mellitus mice.JCI insight · 2020Article
- Article
- Alcohol enhances type 1 interferon-α production and mortality in young mice infected with Mycobacterium tuberculosis.PLoS pathogens · 2018Article
- IL-21 Receptor Signaling Is Essential for Optimal CD4Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- IL-21-dependent expansion of memory-like NK cells enhances protective immune responses against Mycobacterium tuberculosis.Mucosal immunology · 2017Article
- Regulatory T Cell and Forkhead Box Protein 3 as Modulators of Immune Homeostasis.Frontiers in immunology · 2017Review
- A TLR9 agonist promotes IL-22-dependent pancreatic islet allograft survival in type 1 diabetic mice.Nature communications · 2016Article
- Tissue factor expression by myeloid cells contributes to protective immune response against Mycobacterium tuberculosis infection.European journal of immunology · 2016Article
- Challenging Mycobacterium tuberculosis dormancy mechanisms and their immunodiagnostic potential.The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious DiseasesReview
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
In this study, we found that a subpopulation of CD4(+)CD25(+) (85% Foxp3(+)) cells from persons with latent tuberculosis infection (LTBI) inhibits growth of M. tuberculosis (M. tb) in human monocyte-derived macrophages (MDMs). A soluble factor, Rho GDP dissociation inhibitor (D4GDI), produced by apoptotic CD4(+)CD25(+) (85% Foxp3(+)) cells is responsible for this inhibition of M. tb growth in human macrophages and in mice. M. tb-expanded CD4(+C)D25(+)Foxp3(+)D4GDI(+) cells do not produce IL-10, TGF-β and IFN-γ. D4GDI inhibited growth of M. tb in MDMs by enhancing production of IL-1β, TNF-α and ROS, and by increasing apoptosis of M. tb-infected MDMs. D4GDI was concentrated at the site of disease in tuberculosis patients, with higher levels detected in pleural fluid than in serum. However, in response to M. tb, PBMC from tuberculosis patients produced less D4GDI than PBMC from persons with LTBI. M. tb-expanded CD4+CD25+ (85% Foxp3(+)) cells and D4GDI induced intracellular M. tb to express the dormancy survival regulator DosR and DosR-dependent genes, suggesting that D4GDI induces a non-replicating state in the pathogen. Our study provides the first evidence that a subpopulation of CD4(+)CD25(+) (85% Foxp3+) cells enhances immunity to M. tb, and that production of D4GDI by this subpopulation inhibits M. tb growth.
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