ArticleInfection and immunity2003
Toll-like receptor 4-defective C3H/HeJ mice are not more susceptible than other C3H substrains to infection with Mycobacterium tuberculosis.
Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- Single-cell profiling reveals that dynamic lung immune responses distinguish protection from susceptibility to tuberculosis.PLoS pathogens · 2026Article
- A CD40-OX40 co-stimulatory circuit orchestrates protective CD4Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- The ubiquitin ligase CBL and Fas-associated factor 2 cooperate to regulate the innate immune response to M. tuberculosis.PLoS pathogens · 2026Article
- How macrophage heterogeneity affects tuberculosis disease and therapy.Nature reviews. Immunology · 2025Review
- Pathogenic role for CD101-negative neutrophils in the type I interferon-mediated immunopathogenesis of tuberculosis.Cell reports · 2025Article
- TLR4 modulates simvastatin's impact on HDL cholesterol and glycemic control.Frontiers in pharmacology · 2025Article
- The balance between antiviral and antibacterial responses duringbioRxiv : the preprint server for biology · 2024Article
- Comparative Analysis of miRNA Expression after Whole-Body Irradiation Across Three Strains of Mice.Radiation research · 2023Article
- The versatile electric condition in mouse embryos for genome editing using a three-step square-wave pulse electroporator.Experimental animals · 2022Article
- Review
- Underwhelming or Misunderstood? Genetic Variability of Pattern Recognition Receptors in Immune Responses and Resistance toFrontiers in immunology · 2021Review
- Role of Toll-Like Receptors in Tuberculosis Infection.Jundishapur journal of microbiology · 2016Article
- Alopecia areata: Animal models illuminate autoimmune pathogenesis and novel immunotherapeutic strategies.Autoimmunity reviews · 2016Review
- Genomic landscapes of endogenous retroviruses unveil intricate genetics of conventional and genetically-engineered laboratory mouse strains.Experimental and molecular pathology · 2016Article
- TIM3 Mediates T Cell Exhaustion during Mycobacterium tuberculosis Infection.PLoS pathogens · 2016Article
- Interaction of Pattern Recognition Receptors with Mycobacterium Tuberculosis.Journal of clinical immunology · 2015Review
- Virulence-Dependent Alterations in the Kinetics of Immune Cells during Pulmonary Infection by Mycobacterium tuberculosis.PloS one · 2015Article
- In search of a new paradigm for protective immunity to TB.Nature reviews. Microbiology · 2014Review
- Acceleration of tuberculosis treatment by adjunctive therapy with verapamil as an efflux inhibitor.American journal of respiratory and critical care medicine · 2013Article
- Mycobacterium tuberculosis Strains Are Differentially Recognized by TLRs with an Impact on the Immune Response.PloS one · 2013Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Mycobacterium tuberculosis produces a variety of molecules capable of activating Toll-like receptors, a family of pattern recognition receptors expressed by macrophages and a variety of other cells. To determine whether Toll-like receptor 4 (TLR4) was critical in resistance to M. tuberculosis infection, we compared the morbidity and mortality of TLR4-defective C3H/HeJ mice to those of TLR4-sufficient C3H mouse substrains. TLR4-defective C3H/HeJ mice and TLR4-sufficient C3H/HeSnJ, C3HeB/FeJ, and C3H/HeOuJ mice were infected by the aerosol route with M. tuberculosis. TLR4-defective C3H/HeJ mice had levels of cytokines in their bronchoalveolar lavage fluids and in vitro mycobacterial antigen-specific recall responses similar to those of other C3H mouse substrains. In addition, bacterial replication and long-term survival of mice following infection appeared to be independent of TLR4. Interestingly, C3HeB/FeJ mice were significantly more susceptible to M. tuberculosis infection, indicating that genetic heterogeneity among inbred C3H mouse substrains modifies resistance to infection. Therefore, cautious interpretation is required when the C3H/HeJ strain is used as a model of a TLR4-defective mouse strain, as there are significant allelic differences between C3H/HeJ and other C3H mouse substrains in response to M. tuberculosis infection. With this caveat, our data indicate that TLR4 may not be required for optimal immunity of mice to M. tuberculosis.
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