ArticleThe Journal of clinical investigation2016
Lymphatic endothelial cells are a replicative niche for Mycobacterium tuberculosis.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
68 citing papers in PubMed, 104 citations in OpenAlex.
- The crosstalk between lymphatic endothelial cells and immune cells in Physiological and Pathological conditions.Cellular and molecular life sciences : CMLS · 2026Review
- An overview on central nervous system tuberculosis (CNS-TB) focusing on cognitive impairments.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026Review
- From defense to disease: the multifaceted role of lymphatics during infection.Journal of immunology (Baltimore, Md. : 1950) · 2025Review
- Tertiary Lymphoid Structures in Tuberculosis: Persistence, Protection, and Pathology.Immunological reviews · 2025Review
- Article
- Lymphatic transport in anti-tumor immunity and metastasis.The Journal of experimental medicine · 2025Review
- Expanding the field of view - a simple approach for interactive visualisation of electron microscopy data.Journal of cell science · 2024Article
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- Intestinal lymphangiectasia: Understanding the bigger picture.World journal of clinical cases · 2024Article
- Accelerating data sharing and reuse in volume electron microscopy.Nature cell biology · 2024Article
- Next-Gen Dual Transcriptomics for Adult Extrapulmonary Tuberculosis Biomarkers and Host-Pathogen Interplay in Human Cells: A Strategic Review.Indian journal of microbiology · 2024Review
- miR-4687-5p Affects Intracellular Survival ofMicroorganisms · 2024Article
- Lymphatic vessel: origin, heterogeneity, biological functions, and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Autophagy and the pancreas: Healthy and disease states.Frontiers in cell and developmental biology · 2024Review
- Peroxisomal ROS control cytosolic Mycobacterium tuberculosis replication in human macrophages.The Journal of cell biology · 2023Article
- Article
- Serial Block Face-Scanning Electron Microscopy as a Burgeoning Technology.Advanced biology · 2023Review
- Dimethyl itaconate is effective in host-directed antimicrobial responses against mycobacterial infections through multifaceted innate immune pathways.Cell & bioscience · 2023Article
- Early innate cell interactions withFrontiers in immunology · 2023Review
- Role of MHC class I pathways inFrontiers in cellular and infection microbiology · 2023Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
Abstract
In extrapulmonary tuberculosis, the most common site of infection is within the lymphatic system, and there is growing recognition that lymphatic endothelial cells (LECs) are involved in immune function. Here, we identified LECs, which line the lymphatic vessels, as a niche for Mycobacterium tuberculosis in the lymph nodes of patients with tuberculosis. In cultured primary human LECs (hLECs), we determined that M. tuberculosis replicates both in the cytosol and within autophagosomes, but the bacteria failed to replicate when the virulence locus RD1 was deleted. Activation by IFN-γ induced a cell-autonomous response in hLECs via autophagy and NO production that restricted M. tuberculosis growth. Thus, depending on the activation status of LECs, autophagy can both promote and restrict replication. Together, these findings reveal a previously unrecognized role for hLECs and autophagy in tuberculosis pathogenesis and suggest that hLECs are a potential niche for M. tuberculosis that allows establishment of persistent infection in lymph nodes.
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Identifiers
What OpenQuestion holds
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.