ReviewCellular & molecular immunology2017
Innate immunity in tuberculosis: host defense vs pathogen evasion.
Review in Cellular & molecular immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 305 papers, 1 of them a synthesis that pooled it.
What it found
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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
305 citing papers in PubMed, 1 synthesis or guideline pooled it, 522 citations in OpenAlex.
- Interplay of autophagy and Th1/Th2-mediated macrophage polarization in host-pathogen dynamics.Frontiers in cellular and infection microbiology · 2025Pooled it
- Activation of the Nuclear Factor Kappa-light-chain-enhancer of Activated B-cells Pathway Induces a Pro-inflammatory Network in Patients with Pulmonary Tuberculosis.Annals of African medicine · 2026Article
- Transmembrane delivery of antimicrobial peptides by engineered eCIS into macrophages for intracellular mycobacteria elimination.Science advances · 2026Article
- Antigen 85B ofVaccines · 2026Review
- Construction of RecombinantPathogens (Basel, Switzerland) · 2026Article
- cAMP-response element binding protein (CREB)-mediated glycolysis enhancement promotes apoptosis of RAW264.7 macrophages infected with BCG under high glucose conditions.BMC microbiology · 2026Article
- TRIM47 catalyzes MAVS SUMOylation to safeguard chronic viral infections and tissue inflammation.Cell communication and signaling : CCS · 2026Article
- The Sialomucin CD43 Drives Tuberculosis Immunopathology Across Different Host Genetic Backgrounds.Inflammation · 2026Article
- Small RNA ASpks2 promotes Mycobacterium tuberculosis survival in macrophages via targeting polyketide synthase 2.The Journal of biological chemistry · 2026Article
- Immune endotypes in tuberculosis: Keys to decoding disease complexity.Journal of internal medicine · 2026Review
- BTNL2 Inhibits Pyroptosis in H37Ra-Infected Macrophages by Maintaining Mitochondrial Homeostasis.Microorganisms · 2026Article
- A temporal dialogue between the circadian clock and chronic inflammatory diseases.Disease models & mechanisms · 2026Review
- VEGFR Blockade ReducesCells · 2026Article
- From bench to bedside: advances in cell therapy for tuberculosis treatment.Stem cell research & therapy · 2026Review
- Cutaneous Tuberculosis in the Modern Era: A Case of Lupus Vulgaris with Surgical Management and a Review of Clinical Spectrum, Diagnostic Challenges, and Malignant Potential.Journal of clinical medicine · 2026Article
- The role and mechanisms of multiple immunoregulatory cells in pulmonary tuberculosis.Frontiers in immunology · 2026Review
- Immunopathological signatures in congenital tuberculosis-a case-matched study.Frontiers in immunology · 2026Article
- The mechanism regulating the cytotoxicity of γδ T cells activated by mycobacterium tuberculosis heat-resistant antigen based on RNA-seq analysis.Frontiers in immunology · 2026Article
- Single-Cell Insights Into Macrophage Subtypes in Pulmonary Infections.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Macrophage states and polarization duringFrontiers in cellular and infection microbiology · 2026Review
245 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
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The major innate immune cell types involved in tuberculosis (TB) infection are macrophages, dendritic cells (DCs), neutrophils and natural killer (NK) cells. These immune cells recognize the TB-causing pathogen Mycobacterium tuberculosis (Mtb) through various pattern recognition receptors (PRRs), including but not limited to Toll-like receptors (TLRs), Nod-like receptors (NLRs) and C-type lectin receptors (CLRs). Upon infection by Mtb, the host orchestrates multiple signaling cascades via the PRRs to launch a variety of innate immune defense functions such as phagocytosis, autophagy, apoptosis and inflammasome activation. In contrast, Mtb utilizes numerous exquisite strategies to evade or circumvent host innate immunity. Here we discuss recent research on major host innate immune cells, PRR signaling, and the cellular functions involved in Mtb infection, with a specific focus on the host's innate immune defense and Mtb immune evasion. A better understanding of the molecular mechanisms underlying host-pathogen interactions could provide a rational basis for the development of effective anti-TB therapeutics.
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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.