ArticleOncotarget2016
Protein phosphatase, Mg2+/Mn2+-dependent 1A controls the innate antiviral and antibacterial response of macrophages during HIV-1 and Mycobacterium tuberculosis infection.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Article
- PPM1B utilizes a trinuclear metal architecture for phosphatase activity.bioRxiv : the preprint server for biology · 2026Article
- Macrophage states and polarization duringFrontiers in cellular and infection microbiology · 2026Review
- Effect of Kinases in Extracellular Vesicles from HIV-1-Infected Cells on Bystander Cells.Cells · 2025Article
- Tenofovir-tethered gold nanoparticles as a novel multifunctional long-acting anti-HIV therapy to overcome deficient drug delivery-: an in vivo proof of concept.Journal of nanobiotechnology · 2023Article
- Multiple CD59 Polymorphisms in Chinese Patients withJournal of immunology research · 2023Article
- Article
- Article
- A comprehensive overview of PPM1A: From structure to disease.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- Protein phosphatases in TLR signaling.Cell communication and signaling : CCS · 2021Review
- T cell-tropic HIV efficiently infects alveolar macrophages through contact with infected CD4+ T cells.Scientific reports · 2021Article
- Article
- The tetraspanin CD151 marks a unique population of activated human T cells.Scientific reports · 2020Article
- Knockdown of MgExperimental and therapeutic medicine · 2020Article
- Protein Kinase R Restricts the Intracellular Survival ofFrontiers in microbiology · 2020Article
- Cytomegalovirus promotes intestinal macrophage-mediated mucosal inflammation through induction of Smad7.Mucosal immunology · 2018Article
- Tetraspanin blockage reduces exosome-mediated HIV-1 entry.Archives of virology · 2018Article
- The phosphatase PPM1A controls monocyte-to-macrophage differentiation.Scientific reports · 2018Article
- CD151 Expression Is Associated with a Hyperproliferative T Cell Phenotype.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- CD4+ T cells from HIV-1 patients with impaired Th1 effector responses to Mycobacterium tuberculosis exhibit diminished histone and nucleoprotein signatures.Clinical immunology (Orlando, Fla.) · 2017Article
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Authors and funding
8 authors.
Funding
Abstract
Co-infection with HIV-1 and Mycobacterium tuberculosis (Mtb) is a major public health issue. While some research has described how each pathogen accelerates the course of infection of the other pathogen by compromising the immune system, very little is known about the molecular biology of HIV-1/Mtb co-infection at the host cell level. This is somewhat surprising, as both pathogens are known to replicate and persist in macrophages. We here identify Protein Phosphatase, Mg2+/Mn2+-dependent 1A (PPM1A) as a molecular link between Mtb infection and increased HIV-1 susceptibility of macrophages. We demonstrate that both Mtb and HIV-1 infection induce the expression of PPM1A in primary human monocyte/macrophages and THP-1 cells. Genetic manipulation studies revealed that increased PPMA1 expression rendered THP-1 cells highly susceptible to HIV-1 infection, while depletion of PPM1A rendered them relatively resistant to HIV-1 infection. At the same time, increased PPM1A expression abrogated the ability of THP-1 cells to respond to relevant bacterial stimuli with a proper cytokine/chemokine secretion response, blocked their chemotactic response and impaired their ability to phagocytose bacteria. These data suggest that PPM1A, which had previously been shown to play a role in the antiviral response to Herpes Simplex virus infection, also governs the antibacterial response of macrophages to bacteria, or at least to Mtb infection. PPM1A thus seems to play a central role in the innate immune response of macrophages, implying that host directed therapies targeting PPM1A could be highly beneficial, in particular for HIV/Mtb co-infected patients.
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