ArticleThe Journal of clinical investigation2003
CD44 is a macrophage binding site for Mycobacterium tuberculosis that mediates macrophage recruitment and protective immunity against tuberculosis.
Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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.
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Who cites it
44 citing papers in PubMed, 115 citations in OpenAlex.
- Plasma protein biomarkers predictive of progression to active tuberculosis among close contacts of patients with tuberculosis.iScience · 2026Article
- Plasma proteomics for biomarker discovery in childhood tuberculosis.Nature communications · 2025Article
- Association between hematological inflammatory markers and latent TB infection: insights from NHANES 2011-2012 and transcriptomic data.Frontiers in cellular and infection microbiology · 2025Article
- Macrophage migration inhibitory factor-CD74 axis drives vascular smooth muscle cell-induced M1 macrophage polarization to exacerbate intracranial aneurysm inflammation.Frontiers in immunology · 2025Article
- Genomic evidence for adaptation to tuberculosis in the Andes before European contact.iScience · 2023Article
- Genomic variants-driven drug repurposing for tuberculosis by utilizing the established bioinformatic-based approach.Biochemistry and biophysics reports · 2022Article
- Blockade of the pentraxin 3/CD44 interaction attenuates lung injury-induced fibrosis.Clinical and translational medicine · 2022Article
- CD44 receptor targeted nanoparticles augment immunity against tuberculosis in mice.Journal of controlled release : official journal of the Controlled Release Society · 2022Article
- Proteomic networks associated with tumor-educated macrophage polarization and cytotoxicity potentiated by heat-killed tuberculosis.Scientific reports · 2022Article
- Host MKRN1-Mediated Mycobacterial PPE Protein Ubiquitination Suppresses Innate Immune Response.Frontiers in immunology · 2022Article
- Antituberculosis Targeted Drug Delivery as a Potential Future Treatment Approach.Antibiotics (Basel, Switzerland) · 2021Review
- Evolution of Drug-ResistantFrontiers in microbiology · 2021Review
- Aptamers: An Emerging Tool for Diagnosis and Therapeutics in Tuberculosis.Frontiers in cellular and infection microbiology · 2021Review
- PE_PGRS31-S100A9 Interaction Promotes Mycobacterial Survival in Macrophages Through the Regulation of NF-κB-TNF-α Signaling and Arachidonic Acid Metabolism.Frontiers in microbiology · 2020Article
- The CD44-HA axis and inflammation in atherosclerosis: A temporal perspective.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
- Pursuing Intracellular Pathogens with Hyaluronan. From a 'Pro-Infection' Polymer to a Biomaterial for 'Trojan Horse' Systems.Molecules (Basel, Switzerland) · 2018Review
- Article
- Identification potential biomarkers in pulmonary tuberculosis and latent infection based on bioinformatics analysis.BMC infectious diseases · 2016Article
- A Group of Novel Serum Diagnostic Biomarkers for Multidrug-Resistant Tuberculosis by iTRAQ-2D LC-MS/MS and Solexa Sequencing.International journal of biological sciences · 2016Article
- Blood Groups in Infection and Host Susceptibility.Clinical microbiology reviews · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell migration and phagocytosis are both important for controlling Mycobacterium tuberculosis infection and are critically dependent on the reorganization of the cytoskeleton. Since CD44 is an adhesion molecule involved in inflammatory responses and is connected to the actin cytoskeleton, we investigated the role of CD44 in both these processes. Macrophage (Mphi) recruitment into M. tuberculosis-infected lungs and delayed-type hypersensitivity sites was impaired in CD44-deficient (CD44(-/-)) mice. In addition, the number of T lymphocytes and the concentration of the protective key cytokine IFN-gamma were reduced in the lungs of infected CD44(-/-) mice. The production of IFN-gamma by splenocytes of CD44(-/-) mice was profoundly increased upon antigen-specific stimulation. Flow cytometry analysis revealed that soluble CD44 can directly bind to virulent M. tuberculosis. Mycobacteria also interacted with Mphi-associated CD44, as reflected by reduced binding and internalization of bacilli by CD44(-/-) Mphis. This suggests that CD44 is a receptor on Mphis for binding of M. tuberculosis. CD44(-/-) mice displayed a decreased survival and an enhanced mycobacterial outgrowth in lungs and liver during pulmonary tuberculosis. In summary, we have identified CD44 as a new Mphi binding site for M. tuberculosis that mediates mycobacterial phagocytosis, Mphi recruitment, and protective immunity against pulmonary tuberculosis.
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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.