Helminth Co-Infections and Tuberculosis Immunology
Summary
In regions where tuberculosis and helminthiasis are co-endemic, concomitant worm infections can profoundly reshape host immunity against Mycobacterium tuberculosis. Helminths typically drive strong type 2 helper T cell (Th2) and regulatory T cell (Treg) responses, characterised by interleukins IL-4, IL-5, IL-10 and transforming growth factor β, which counterbalance the Th1-mediated interferon-γ (IFN-γ) and tumour necrosis factor (TNF) pathways essential for mycobacterial containment and granuloma formation. This immunomodulation may impair vaccine efficacy, delay bacterial clearance and alter clinical presentation. Conversely, persistent Th1 activation during tuberculosis can compromise anti-helminth immunity, illustrating bidirectional interference. Variations in parasite species, worm burden and host genetics influence the magnitude of immune skewing. From a public health standpoint, helminth-driven suppression of protective antimycobacterial responses underscores the need for integrated control strategies, combining deworming, vaccination and tailored therapeutic regimens to optimise outcomes in co-infected populations.
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Helminth Co-Infections and Tuberculosis Immunology publication trend
The graph below shows the total number of articles in helminth co-infections and tuberculosis immunology across all publications each year (not limited to Nature Index journals).
Technical terms
Th1 response: A cell-mediated immune reaction driven by IFN-γ and TNF-α that activates macrophages to contain and kill intracellular pathogens such as Mycobacterium tuberculosis.
Th2 response: An immune pathway characterised by IL-4, IL-5 and IL-13 that promotes antibody production and eosinophil activation, often elicited by helminth infections.
Regulatory T cell (Treg): A subset of CD4+ T cells that secrete IL-10 and TGF-β to dampen excessive inflammation and maintain immune homeostasis, but may also inhibit protective antimicrobial responses.
Cytokine: A small secreted protein, such as IFN-γ, IL-4 or IL-10, that mediates communication between immune cells and orchestrates the nature and magnitude of immune responses.
Granuloma: A structured aggregate of immune cells, including macrophages and lymphocytes, that walls off Mycobacterium tuberculosis to limit its spread but can also contribute to tissue damage.
References
- Cytokine Responses during Mycobacterium tuberculosis H37Rv and Ascaris lumbricoides Costimulation Using Human THP-1 and Jurkat Cells, and a Pilot Human Tuberculosis and Helminth Coinfection Study. Microorganisms (2023).
- Helminth species-specific effects on IFN-γ producing T cells during active and latent tuberculosis. PLOS Neglected Tropical Diseases (2023).
- Immunological and Haematological Relevance of Helminths and Mycobacterium tuberculosis Complex Coinfection among Newly Diagnosed Pulmonary Tuberculosis Patients from Bobo-Dioulasso, Burkina Faso. Biomedicines (2024).
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