ArticleThe Journal of infectious diseases2009
Mycobacterium tuberculosis interferes with the response to infection by inducing the host EphA2 receptor.
Article in The Journal of infectious diseases, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Emerging host-directed strategies for overcoming drug resistance and immune evasion in Staphylococcus aureus infections.Journal of advanced research · 2026Review
- Granulomatous cellular signatures in nontuberculous and tuberculous mycobacterial infections.Frontiers in microbiology · 2025Article
- Article
- Targeting Host Tyrosine Kinase Receptor EPHA2 Signaling Affects Uropathogen Infection in Human Bladder Epithelial Cells.Pathogens (Basel, Switzerland) · 2022Article
- IL-23 signaling prevents ferroptosis-driven renal immunopathology during candidiasis.Nature communications · 2022Article
- Digenic inheritance of mutations in EPHA2 and SLC26A4 in Pendred syndrome.Nature communications · 2020Article
- Host-directed kinase inhibitors act as novel therapies against intracellular Staphylococcus aureus.Scientific reports · 2019Article
- Emerging Roles for Eph Receptors and Ephrin Ligands in Immunity.Frontiers in immunology · 2019Review
- G908R NOD2 variant in a family with sarcoidosis.Respiratory research · 2018Article
- Primary macrophages and J774 cells respond differently to infection with Mycobacterium tuberculosis.Scientific reports · 2017Article
- EphA2 activation promotes the endothelial cell inflammatory response: a potential role in atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2012Article
- Imaging tuberculosis with endogenous beta-lactamase reporter enzyme fluorescence in live mice.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundMycobacterium tuberculosis is an unusual pathogen, persisting for years in infected persons despite an immune response. Erythropoietin-producing hepatoma (Eph) receptors are critical for tissue organization. One hallmark of tuberculosis is the presence of granulomas consisting of organized immune cells. The importance of granuloma structure makes it likely that Eph receptors play a role in immunity to tuberculosis.
methodsWe infected mice with low doses of M. tuberculosis by the aerosol method and examined the effects on ephA gene expression, pathology, composition of lymphocytes in the lungs (by flow cytometry), migration of CD4+ and CD8+ T cells, and numbers of cytokine-expressing cells.
resultsMice infected with M. tuberculosis displayed higher expression of ephA1 and ephA2 as well as ephrinA1, which encodes the ligand for EphA1 and EphA2. Interestingly, ephA2-/- mice displayed greater pathology, greater accumulation of T cells and dendritic cells, and higher levels of proinflammatory cytokines than did normal C57BL/6 mice. Furthermore, T cells from ephA2-/- mice migrated more efficiently than did those from C57BL/6 mice.
conclusionsThese observations suggest that ephA-related genes may provide a mechanism that M. tuberculosis uses to circumvent the host response, given that accumulation of T cells appears to be due to the inhibition of immune cell migration by EphA2. Ultimately, the absence of ephA2 results in greater clearance of M. tuberculosis during the chronic phase of infection, suggesting that induction of ephA2 is important for the survival of M. tuberculosis during latency.
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