ArticleThe Journal of infectious diseases2013
Phosphorylation of mitogen-activated protein kinases contributes to interferon γ production in response to Mycobacterium tuberculosis.
Article in The Journal of infectious diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- PGE2 displays immunosuppressive effects during human active tuberculosis.Scientific reports · 2021Trial
- Cell death pathways in response toInfection and immunity · 2025Review
- The Impact of IFN-γ Licensing on Mesenchymal Stromal Cells' Mediated Immunoregulation and HLA Class II Expression: Emerging Evidence from In Vitro Results.International journal of molecular sciences · 2025Article
- Macrophage-T cell interactions promote SLAMF1 expression for enhanced TB defense.Nature communications · 2025Article
- Immune-neuroendocrine reactivity and features of tuberculosis in pregnancy.Frontiers in medicine · 2025Review
- Impact of anti-TB drugs on modulations of T-cell-receptor-mediated signaling events in TB pleurisy patients.Frontiers in immunology · 2025Review
- Extensive differential DNA methylation between tuberculosis skin test positive and skin test negative cattle.BMC genomics · 2024Article
- Depletion of essential mycobacterial gene glmM reduces pathogen survival and induces host-protective immune responses against tuberculosis.Communications biology · 2024Article
- Transcriptional Analysis for Tuberculosis in Pregnant Women From the PRegnancy Associated Changes In Tuberculosis Immunology (PRACHITi) Study.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2022Article
- The 1, 2-ethylenediamine SQ109 protects against tuberculosis by promoting M1 macrophage polarization through the p38 MAPK pathway.Communications biology · 2022Article
- Exploring modulations in T-cell receptor-mediated T-cell signaling events in systemic circulation and at local disease site of patients with tubercular pleural effusion: An attempt to understand tuberculosis pathogenesis at the local disease site.Frontiers in medicine · 2022Article
- Deciphering Genetic Susceptibility to Tuberculous Meningitis.Frontiers in neurology · 2022Article
- Splicing factor SRSF1 is essential for CD8 T cell function and host antigen-specific viral immunity.Frontiers in immunology · 2022Article
- microRNAs associated with the pathogenesis and their role in regulating various signaling pathways duringFrontiers in cellular and infection microbiology · 2022Review
- Intranasal immunization with peptide-based immunogenic complex enhances BCG vaccine efficacy in a murine model of tuberculosis.JCI insight · 2021Article
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- A Bumpy Ride of Mycobacterial Phagosome Maturation: Roleplay of Coronin1 Through Cofilin1 and cAMP.Frontiers in immunology · 2021Article
- Antibacterial peptides inhibit MC3T3-E1 cells apoptosis induced by TNF-α through p38 MAPK pathway.Annals of translational medicine · 2020Article
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Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Immune control of Mycobacterium tuberculosis depends on interferon γ (IFN-γ)-producing CD4(+) lymphocytes. Previous studies have shown that T cells from patients with tuberculosis produce less IFN-γ, compared with healthy donors, in response to mycobacterial antigens, although IFN-γ responses to mitogens are preserved. In this work, we found that M. tuberculosis-induced IFN-γ production by human T cells correlated with phosphorylation of the mitogen-activated protein kinases (MAPKs), extracellular signal-regulated kinase (ERK), and p38. Moreover, the majority of IFN-γ-producing T cells expressed signaling lymphocyte activation molecule (SLAM), and SLAM activation further increased ERK phosphorylation. Interestingly, patients with tuberculosis had delayed activation of ERK and p38, and this was most marked in patients with the poorest IFN-γ responses (ie, low responders). Besides, SLAM signaling failed to phosphorylate ERK in low responders. Our findings suggest that activation of p38 and ERK, in part through SLAM, mediates T-cell IFN-γ production in response to M. tuberculosis, a pathway that is defective in patients with tuberculosis.
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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.