Immunology · Cytokines and molecules
TNF-α !
- Molecule
TNF-α is a powerful inflammation signal from macrophages. It holds tuberculosis granulomas together, and blocking it treats arthritis and bowel disease.
Updated 2026-11-01
What it is
Tumour necrosis factor-α is made mainly by macrophages and monocytes, and also by T cells, neutrophils and other cells; it exists as a membrane form and a soluble form, and both are active. It acts on TNFR1 (on almost all nucleated cells) and TNFR2 (mostly immune cells). TNF starts a cascade that includes IL-1 and IL-6, activates endothelium and is needed to build and maintain granulomas.
Function
- Activates endothelium (adhesion molecules) and recruits leukocytes.
- Activates macrophages together with IFN-γ.
- Induces IL-1 and IL-6 and the acute-phase response.
- Can trigger apoptosis of target cells through TNFR1.
Clinical notes
- Rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, juvenile idiopathic arthritis and psoriasis respond to anti-TNF therapy, often combined with methotrexate in RA.
- Crohn disease and ulcerative colitis: infliximab, adalimumab and others.
- Septic shock: TNF is one of the mediators of vasodilation and organ damage.
- Anti-TNF therapy increases serious bacterial, viral and fungal infections; tuberculosis often appears as extrapulmonary or disseminated disease.
- In Colombia and Latin America, where tuberculosis is common, screening and treatment of latent infection before anti-TNF is essential.
In the lab
- Latent tuberculosis screening: tuberculin skin test or interferon-γ release assay, plus chest X-ray.
- Hepatitis B serology before starting.
Test yourself
Think of the answer, then tap the question to see it.
Why must latent tuberculosis be ruled out before an anti-TNF drug?
TNF is needed to keep granulomas intact; blocking it can reactivate dormant Mycobacterium tuberculosis, often as disseminated disease.
How does etanercept differ in structure from infliximab?
Etanercept is a soluble TNFR2 receptor fused to an IgG Fc fragment; infliximab is a chimeric monoclonal antibody against TNF.
Which systemic effects of TNF-α explain septic shock and cachexia?
Vasodilation and capillary leak with low blood pressure, plus loss of appetite and muscle and fat breakdown in chronic inflammation.
Related
- Cytokines: the table to know
- Interleukin-1
- Interleukin-6
- Interferon-γ
- Granulomatous inflammation
- Acute-phase response and fever (CRP, ESR, procalcitonin)
- Tuberculin skin test and IGRA
- Monoclonal antibodies and biologics: naming and targets
- Monocyte and macrophage
Related conditions
- Rheumatoid arthritis
- Sepsis and septic shock
- Crohn disease
- Ulcerative colitis
- Ankylosing spondylitis
- Tuberculosis
Microorganisms
In Pharmacology
Educational content on the immune system; not a treatment or individual vaccination guide and no substitute for a health professional's advice. No doses are given.
Sources: Tumor Necrosis Factor (TNF) Bioactivity at the Site of an Acute Cell-Mediated Immune Response Is Preserved in Rheumatoid Arthritis Patients Responding to Anti-TNF Therapy (Frontiers in Immunology, 2017); Infliximab Injection: MedlinePlus Drug Information (MedlinePlus (U.S. National Library of Medicine), 2025); Etanercept Injection: MedlinePlus Drug Information (MedlinePlus (U.S. National Library of Medicine), 2025); Pro-Inflammatory and Anti-Inflammatory Interleukins in Infectious Diseases: A Comprehensive Review (Tropical Medicine and Infectious Disease (PubMed Central), 2024).
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Representative model, for educational purposes only.