ArticleScientific reports2016
A novel therapeutic strategy of lipidated promiscuous peptide against Mycobacterium tuberculosis by eliciting Th1 and Th17 immunity of host.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Furamidine enhances IL-23-mediated autophagic response through IL-23R-TYK2-STAT3-dependent regulation of intracellular Ca²⁺ level to facilitate mycobacterial clearance in human macrophages.Medical microbiology and immunology · 2025Article
- Progress of single-cell sequencing technology in immunotherapy for tuberculosis.Frontiers in cellular and infection microbiology · 2025Review
- Identification of differentially recognized T cell epitopes in the spectrum of tuberculosis infection.Nature communications · 2024Article
- Immunologic, metabolic and genetic impact of diabetes on tuberculosis susceptibility.Frontiers in immunology · 2023Review
- Photochemically-Mediated Inflammation and Cross-Presentation ofFrontiers in immunology · 2022Article
- Increased susceptibility to pneumonia due to tumour necrosis factor inhibition and prospective immune system rescueFrontiers in cellular and infection microbiology · 2022Review
- Recent Advances in the Development of Protein- and Peptide-Based Subunit Vaccines against Tuberculosis.Cells · 2020Review
- Induction of autophagy through CLEC4E in combination with TLR4: an innovative strategy to restrict the survival ofAutophagy · 2020Article
- Curdlan LimitsFrontiers in microbiology · 2019Article
- The crucial roles of Th17-related cytokines/signal pathways in M. tuberculosis infection.Cellular & molecular immunology · 2018Review
- Bolstering Immunity through Pattern Recognition Receptors: A Unique Approach to Control Tuberculosis.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regardless of the fact that potent drug-regimen is currently available, tuberculosis continues to kill 1.5 million people annually. Tuberculosis patients are not only inflicted by the trauma of disease but they also suffer from the harmful side-effects, immune suppression and drug resistance instigated by prolonged therapy. It is an exigency to introduce radical changes in the existing drug-regime and discover safer and better therapeutic measures. Hence, we designed a novel therapeutic strategy by reinforcing the efficacy of drugs to kill Mtb by concurrently boosting host immunity by L91. L91 is chimera of promiscuous epitope of Acr1 antigen of Mtb and TLR-2 agonist Pam2Cys. The adjunct therapy using drugs and L91 (D-L91) significantly declined the bacterial load in Mtb infected animals. The mechanism involved was through enhancement of IFN-γ(+)TNF-α(+) polyfunctional Th1 cells and IL-17A(+)IFN-γ(+) Th17 cells, enduring memory CD4 T cells and downregulation of PD-1. The down-regulation of PD-1 prevents CD4 T cells from undergoing exhaustion and improves their function against Mtb. Importantly, the immune response observed in animals could be replicated using T cells of tuberculosis patients on drug therapy. In future, D-L91 therapy can invigorate drugs potency to treat tuberculosis patients and reduce the dose and duration of drug-regime.
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