Immunology · Cytokines and molecules
Cytokines: the table to know !
- Topic
Cytokines are small proteins that immune cells use to talk to each other: they switch inflammation on or off and tell other cells what to become.
Updated 2026-11-01
What it is
Cytokines are small secreted proteins (interleukins, interferons, TNF, TGF-β and the chemokines) that act on nearby cells through specific surface receptors. Each one is defined by who makes it, which receptor it uses and what it does; most exam questions ask exactly those three things. Many are now targets of biologic drugs, so the same table explains rheumatoid arthritis, psoriasis, asthma and Crohn disease therapy.
Key facts
- Cytokines act over short distances; chemokines are the subgroup that pulls cells along a gradient (chemotaxis).
- The same cytokine can have several effects (pleiotropy) and different cytokines can share an effect (redundancy).
- Many cytokine receptors signal through JAK kinases and STAT factors, which is why JAK inhibitors block several cytokines at once.
- A cytokine storm is an excessive, body-wide release (for example in sepsis or cytokine release syndrome).
Main cytokines: who makes them, what they do and where they matter in the clinic
| Cytokine | Main source | Main effect | Clinical link |
|---|---|---|---|
| IL-1 | Macrophages, monocytes | Fever, endothelial activation, recruits immune cells | Autoinflammatory fevers, gout flares; anakinra, canakinumab |
| IL-2 | Activated T cells | T-cell proliferation; keeps regulatory T cells alive | Transplant immunosuppression; aldesleukin in some cancers |
| IL-4 | Th2 and T follicular helper cells | Th2 differentiation, IgE class switch | Allergy, asthma, eczema; dupilumab blocks its receptor |
| IL-5 | Th2 cells, ILC2 | Eosinophil maturation and survival | Eosinophilic asthma; mepolizumab, benralizumab |
| IL-6 | Macrophages, T cells, fibroblasts | Acute phase (CRP), fever, plasma cells, Th17 | Rheumatoid arthritis, cytokine release syndrome; tocilizumab |
| IL-8 (CXCL8) | Macrophages, epithelium, mast cells | Brings neutrophils to the site | Pus-rich inflammation; marker in neonatal sepsis studies |
| IL-10 | Regulatory T cells, macrophages | Turns off macrophages and inflammatory cytokines | Defects cause severe colitis; some microbes exploit it |
| IL-12 | Dendritic cells, macrophages | Th1 differentiation, IFN-γ from NK and T cells | Defects in its axis: mycobacterial infections; ustekinumab |
| IL-13 | Th2 cells, ILC2 | Mucus, airway hyperreactivity, remodelling | Asthma, atopic dermatitis; tralokinumab |
| IL-17 | Th17 cells, γδ T cells, ILC3 | Neutrophil recruitment, antimicrobial peptides | Psoriasis, spondyloarthritis; secukinumab |
| IL-23 | Dendritic cells, macrophages | Keeps Th17 cells expanding | Psoriasis, Crohn disease; guselkumab |
| TNF-α | Macrophages (also T cells, others) | Inflammation, granuloma upkeep, septic shock | RA, IBD, psoriasis; anti-TNF after latent TB screening |
| IFN-γ | Th1, NK and CD8 T cells | Activates macrophages, raises MHC class II | Basis of IGRA test; used in chronic granulomatous disease |
| IFN-α/β | Virus-infected cells, plasmacytoid dendritic cells | Antiviral state in neighbouring cells, NK activation | Lupus interferon signature; IFN-β in multiple sclerosis |
| TGF-β | Regulatory T cells and many other cells | Suppresses immune responses, induces Tregs, fibrosis | With IL-6 it drives Th17 cells; airway remodelling |
Test yourself
Think of the answer, then tap the question to see it.
Which three cytokines are the classic endogenous pyrogens?
IL-1, IL-6 and TNF-α, mainly from activated macrophages; IL-6 also drives CRP and other acute-phase proteins in the liver.
Which cytokine drives IgE class switching and which one drives eosinophils?
IL-4 drives the switch to IgE (with IL-13 helping); IL-5 drives eosinophil maturation and survival.
What links IL-12 and IFN-γ?
IL-12 from dendritic cells and macrophages pushes Th1 and NK cells to make IFN-γ, which in turn activates macrophages to kill intracellular microbes such as mycobacteria.
Which test is needed before starting an anti-TNF drug?
Screening for latent tuberculosis (tuberculin skin test or interferon-γ release assay), because blocking TNF can reactivate it.
Related
- Interleukin-1
- Interleukin-2
- IL-4, IL-5 and IL-13 (the Th2 cytokines)
- Interleukin-6
- IL-8 and the chemokines
- IL-10 and TGF-β (the brakes)
- IL-12 and IL-23
- Interleukin-17
- TNF-α
- Interferon-γ
- Type I interferons (α, β)
- Th1, Th2, Th17, Tfh and Treg
- Acute-phase response and fever (CRP, ESR, procalcitonin)
- Monoclonal antibodies and biologics: naming and targets
Related conditions
- Rheumatoid arthritis
- Asthma
- Crohn disease
- Systemic lupus erythematosus
- Tuberculosis
- Sepsis and septic shock
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: Pro-Inflammatory and Anti-Inflammatory Interleukins in Infectious Diseases: A Comprehensive Review (Tropical Medicine and Infectious Disease (PubMed Central), 2024); 21.2 Barrier Defenses and the Innate Immune Response - Anatomy and Physiology 2e | OpenStax (OpenStax, 2022); 21.3 The Adaptive Immune Response: T lymphocytes and Their Functional Types - Anatomy and Physiology 2e | OpenStax (OpenStax, 2022); Regulation of Treg cells by cytokine signaling and co-stimulatory molecules (Frontiers in Immunology, 2024).
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Representative model, for educational purposes only.