ArticlePLoS pathogens2018
STAT3 expression by myeloid cells is detrimental for the T- cell-mediated control of infection with Mycobacterium tuberculosis.
Article in PLoS pathogens, 2018. 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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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Mitochondrial STAT3-mediated suppression of apoptosis constrains antimycobacterial immunity.bioRxiv : the preprint server for biology · 2026Article
- STAT3 Deficiency Alters the Macrophage Activation Pattern and Enhances Matrix Metalloproteinase 9 Expression during Staphylococcal Pneumonia.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Short chain fatty acids facilitate protective immunity by macrophages and T cells during acute fowl adenovirus-4 infection.Scientific reports · 2023Article
- Review
- Intestinal helminth infection transforms the CD4Mucosal immunology · 2022Article
- MSC-ACE2 AmelioratesFrontiers in immunology · 2022Article
- Recent Advances in Host-Directed Therapies for Tuberculosis and Malaria.Frontiers in cellular and infection microbiology · 2022Review
- Novel Role for Macrophage Galactose-Type Lectin-1 to Regulate Innate Immunity againstJournal of immunology (Baltimore, Md. : 1950) · 2021Article
- Transfer transcriptomic signatures for infectious diseases.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Down-regulation of STAT3 enhanced chemokine expression and neutrophil recruitment in biliary atresia.Clinical science (London, England : 1979) · 2021Article
- The GT1-TPS Structural Domain Protein FromFrontiers in immunology · 2021Article
- H. pylori modulates DC functions via T4SS/TNFα/p38-dependent SOCS3 expression.Cell communication and signaling : CCS · 2020Article
- The Toxoplasma gondii virulence factor ROP16 acts in cis and trans, and suppresses T cell responses.The Journal of experimental medicine · 2020Article
- MicroRNA-127 Promotes Anti-microbial Host Defense through Restricting A20-Mediated De-ubiquitination of STAT3.iScience · 2020Article
- Article
- Macrophage Migration Inhibitory Factor (MIF) Is Essential for Type 2 Effector Cell Immunity to an Intestinal Helminth Parasite.Frontiers in immunology · 2019Article
- IL-10/STAT3/SOCS3 Axis Is Involved in the Anti-inflammatory Effect of Benznidazole.Frontiers in immunology · 2019Article
- Host Directed Therapy for Chronic Tuberculosis via Intrapulmonary Delivery of Aerosolized Peptide Inhibitors Targeting the IL-10-STAT3 Pathway.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
STAT3 is a master regulator of the immune responses. Here we show that M. tuberculosis-infected stat3fl/fl lysm cre mice, defective for STAT3 in myeloid cells, contained lower bacterial load in lungs and spleens, reduced granuloma extension but higher levels of pulmonary neutrophils. STAT3-deficient macrophages showed no improved control of intracellular mycobacterial growth. Instead, protection associated to elevated ability of stat3fl/fl lysm cre antigen-presenting cells (APCs) to release IL-6 and IL-23 and to stimulate IL-17 secretion by mycobacteria-specific T cells. The increased IL-17 secretion accounted for the improved control of infection since neutralization of IL-17 receptor A in stat3fl/fl lysm cre mice hampered bacterial control. APCs lacking SOCS3, which inhibits STAT3 activation via several cytokine receptors, were poor inducers of priming and of the IL-17 production by mycobacteria-specific T cells. In agreement, socs3fl/fl cd11c cre mice deficient of SOCS3 in DCs showed increased susceptibility to M. tuberculosis infection. While STAT3 in APCs hampered IL-17 responses, STAT3 in mycobacteria-specific T cells was critical for IL-17 secretion, while SOCS3 in T cells impeded IL-17 secretion. Altogether, STAT3 signalling in myeloid cells is deleterious in the control of infection with M. tuberculosis.
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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.