ArticleAutophagy2017
IL17A augments autophagy in Mycobacterium tuberculosis-infected monocytes from patients with active tuberculosis in association with the severity of the disease.
Article in Autophagy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 47 citations in OpenAlex.
- PGE2 displays immunosuppressive effects during human active tuberculosis.Scientific reports · 2021Trial
- MAPK signaling pathways in host immune regulation during Mycobacterium tuberculosis infection.Frontiers in immunology · 2026Review
- The diagnostic value and validation of IL-22 combimed with sCD40L in tuberculosis pleural effusion.BMC immunology · 2024Article
- Review
- Functional Analysis of Genes inIndian journal of microbiology · 2024Review
- HervD Atlas: a curated knowledgebase of associations between human endogenous retroviruses and diseases.Nucleic acids research · 2024Article
- Rare Case Report of Primary Active Pulmonary Tuberculosis During Ixekizumab Treatment for Plaque Psoriasis.Clinical, cosmetic and investigational dermatology · 2024Article
- Identification of Differential Circular RNA Expression Profiles and Functional Networks in Human Macrophages Induced by Virulent and AvirulentInternational journal of molecular sciences · 2023Article
- Secukinumab plays a synergistic role with starvation therapy in promoting autophagic cell death of hepatocellular carcinoma via inhibiting IL-17A-increased BCL2 level.In vitro cellular & developmental biology. Animal · 2023Article
- IL-17A inhibits the degradation of RANKL in osteoblasts by inhibiting BCL2-Beclin1-autophagy signaling.In vitro cellular & developmental biology. Animal · 2023Article
- Beyond the Clinic: The Activation of Diverse Cellular and Humoral Factors Shapes the Immunological Status of Patients with Active Tuberculosis.International journal of molecular sciences · 2023Review
- Circulating Monocyte-Like Myeloid Derived Suppressor Cells and CD16 Positive Monocytes Correlate With Immunological Responsiveness of Tuberculosis Patients.Frontiers in cellular and infection microbiology · 2022Article
- Exploring the association between Th17 pathway gene polymorphisms and pulmonary tuberculosis.Frontiers in immunology · 2022Article
- Mycoplasma bovis subverts autophagy to promote intracellular replication in bovine mammary epithelial cells cultured in vitro.Veterinary research · 2021Article
- Autophagy in major human diseases.The EMBO journal · 2021Review
- Article
- Shedding Light on Autophagy During Human Tuberculosis. A Long Way to Go.Frontiers in cellular and infection microbiology · 2021Review
- An Integrative Network Approach to Identify Common Genes for the Therapeutics in Tuberculosis and Its Overlapping Non-Communicable Diseases.Frontiers in pharmacology · 2021Article
- Article
- Vitamin D-Cathelicidin Axis: at the Crossroads between Protective Immunity and Pathological Inflammation during Infection.Immune network · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During mycobacterial infection, macroautophagy/autophagy, a process modulated by cytokines, is essential for mounting successful host responses. Autophagy collaborates with human immune responses against Mycobacterium tuberculosis (Mt) in association with specific IFNG secreted against the pathogen. However, IFNG alone is not sufficient to the complete bacterial eradication, and other cytokines might be required. Actually, induction of Th1 and Th17 immune responses are required for protection against Mt. Accordingly, we showed that IL17A and IFNG expression in lymphocytes from tuberculosis patients correlates with disease severity. Here we investigate the role of IFNG and IL17A during autophagy in monocytes infected with Mt H37Rv or the mutant MtΔRD1. Patients with active disease were classified as high responder (HR) or low responder (LR) according to their T cell responses against Mt. IL17A augmented autophagy in infected monocytes from HR patients through a mechanism that activated MAPK1/ERK2-MAPK3/ERK1 but, during infection of monocytes from LR patients, IL17A had no effect on the autophagic response. In contrast, addition of IFNG to infected monocytes, increased autophagy by activating MAPK14/p38 α both in HR and LR patients. Interestingly, proteins codified in the RD1 region did not interfere with IFNG and IL17A autophagy induction. Therefore, in severe tuberculosis patients' monocytes, IL17A was unable to augment autophagy because of a defect in the MAPK1/3 signaling pathway. In contrast, both IFNG and IL17A increased autophagy levels in patients with strong immunity to Mt, promoting mycobacterial killing. Our findings might contribute to recognize new targets for the development of novel therapeutic tools to fight the pathogen.
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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.