ArticleProceedings of the National Academy of Sciences of the United States of America2013
Macrophage migration inhibitory factor (MIF) is a critical mediator of the innate immune response to Mycobacterium tuberculosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 3 of them syntheses that pooled it.
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Who cites it
75 citing papers in PubMed, 3 syntheses or guidelines pooled it, 119 citations in OpenAlex.
- Association of Macrophage Migration Inhibitory Factor-794 CATT Microsatellite Polymorphism With Tuberculosis Risk: A Systematic Review and Meta-Analysis.Pulmonary medicine · 2026Pooled it
- Systematic review of innate immune responses againstFrontiers in immunology · 2024Pooled it
- Association between the MIF-173G/C Polymorphism and Serum MIF levels with Pulmonary Tuberculosis: A Meta-analysis.Scientific reports · 2017Pooled it
- Mycobacterial α-glucans hijack dectin-1 to facilitate intracellular bacterial survival.Science immunology · 2026Article
- Single-cell transcriptomic profiling of cerebrospinal fluid reveals immune-cell heterogeneity and multicompartment MIF/CD74-related communication in tuberculous and purulent meningitis.Frontiers in cellular and infection microbiology · 2026Article
- Macrophage migration inhibitory factor: Exploring physiological roles and comparing health benefits against oncogenic and autoimmune risks (Review).International journal of molecular medicine · 2025Review
- Single-cell transcriptome analysis reveals the dysregulated monocyte state associated with tuberculosis progression.BMC infectious diseases · 2025Article
- Granulomatous cellular signatures in nontuberculous and tuberculous mycobacterial infections.Frontiers in microbiology · 2025Article
- Macrophage migration inhibitory factor (MIF) and the tumor ecosystem: a tale of inflammation, immune escape, and tumor growth.Frontiers in immunology · 2025Review
- The distinct functions of MIF in inflammatory cardiomyopathy.Frontiers in immunology · 2025Review
- Article
- The Role of Macrophage Migration Inhibitory Factor (MIF) and D-Dopachrome Tautomerase (D-DT/MIF-2) in Infections: A Clinical Perspective.Biomedicines · 2023Review
- Role of pattern recognition receptors in sensingHeliyon · 2023Review
- Article
- Modulatory role of macrophage migration inhibitory factor on cytokines and clinical features of sarcoidosis.Scientific reports · 2022Article
- Chinese Medicine Meets Conventional Medicine in Targeting COVID-19 Pathophysiology, Complications and Comorbidities.Chinese journal of integrative medicine · 2022Article
- Immunopathogenic overlap between COVID-19 and tuberculosis identified from transcriptomic meta-analysis and human macrophage infection.iScience · 2022Article
- The IL-25-dependent tuft cell circuit driven by intestinal helminths requires macrophage migration inhibitory factor (MIF).Mucosal immunology · 2022Article
- The immune-suppressive landscape in lepromatous leprosy revealed by single-cell RNA sequencing.Cell discovery · 2022Article
- MIF but not MIF-2 recruits inflammatory macrophages in an experimental polymicrobial sepsis model.The Journal of clinical investigation · 2021Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 8 institutions in 2 countries.
Funding
Abstract
Macrophage migration inhibitory factor (MIF), an innate cytokine encoded in a functionally polymorphic genetic locus, contributes to detrimental inflammation but may be crucial for controlling infection. We explored the role of variant MIF alleles in tuberculosis. In a Ugandan cohort, genetic low expressers of MIF were 2.4-times more frequently identified among patients with Mycobacterium tuberculosis (TB) bacteremia than those without. We also found mycobacteria-stimulated transcription of MIF and serum MIF levels to be correlated with MIF genotype in human macrophages and in a separate cohort of US TB patients, respectively. To determine mechanisms for MIF's protective role, we studied both aerosolized and i.v. models of mycobacterial infection and observed MIF-deficient mice to succumb more quickly with higher organism burden, increased lung pathology, and decreased innate cytokine production (TNF-α, IL-12, IL-10). MIF-deficient animals showed increased pulmonary neutrophil accumulation but preserved adaptive immune response. MIF-deficient macrophages demonstrated decreased cytokine and reactive oxygen production and impaired mycobacterial killing. Transcriptional investigation of MIF-deficient macrophages revealed reduced expression of the pattern recognition receptor dectin-1; restoration of dectin-1 expression recovered innate cytokine production and mycobacterial killing. Our data place MIF in a crucial upstream position in the innate immune response to mycobacteria and suggest that commonly occurring low expression MIF alleles confer an increased risk of TB disease in some populations.
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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.