Immunology · Adaptive immunity
Th1, Th2, Th17, Tfh and Treg !
- Topic
Helper T cells specialize into types that fight different germs, each with its own set of chemical signals.
Updated 2026-11-01
What it is
After activation, CD4 helper T cells differentiate according to the cytokines around them. Each subset has a master transcription factor and signature cytokines that suit a type of threat: Th1 for intracellular microbes, Th2 for helminths, Th17 for extracellular bacteria and fungi at mucosal surfaces, Tfh for helping B cells make antibodies, and Treg for keeping responses in check. When a subset is excessive or misdirected, it underlies typical diseases.
Key facts
- IFN-γ inhibits Th2 cells and IL-4 inhibits Th1 cells, so the response tends to polarize.
- Treg cells are CD4+ CD25+ FOXP3+.
- Hyper-IgE syndrome with STAT3 mutation lacks Th17 cells: skin abscesses and candidiasis.
- In leprosy, a Th1 response gives the tuberculoid form and a Th2-skewed response the lepromatous form.
CD4 helper subsets
| Subset | Induced by | Signature cytokines | Main function | Disease when excessive (or missing) |
|---|---|---|---|---|
| Th1 (T-bet) | IL-12, IFN-γ | IFN-γ, IL-2 | Activates macrophages and CD8 T cells; intracellular microbes | Type IV hypersensitivity, granulomas; some organ-specific autoimmunity |
| Th2 (GATA-3) | IL-4 | IL-4, IL-5, IL-13 | IgE class switch, eosinophils, mucus; helminths | Allergy, atopic asthma |
| Th17 (RORγt) | TGF-β plus IL-6 (IL-23 sustains) | IL-17, IL-22 | Recruits neutrophils; mucosal defense against bacteria and Candida | Psoriasis, inflammatory bowel disease; when missing, chronic mucocutaneous candidiasis |
| Tfh (Bcl-6) | IL-6, IL-21 | IL-21 (plus CD40L, CXCR5) | Helps B cells in germinal centers: class switch and affinity maturation | High-affinity autoantibodies, as in lupus |
| Treg (FOXP3) | TGF-β, IL-2 | IL-10, TGF-β | Suppresses other T cells; peripheral tolerance | When missing, IPEX syndrome; excess can protect tumors |
Clinical notes
- Defects in the IL-12/IFN-γ axis cause disseminated mycobacterial infections.
- Biologic drugs target subset cytokines: anti-IL-17 and anti-IL-23 in psoriasis, anti-IL-5 and anti-IL-4 receptor in severe eosinophilic or allergic disease.
- IPEX (FOXP3 mutation): early severe enteropathy, type 1 diabetes in infancy and eczema.
Test yourself
Think of the answer, then tap the question to see it.
Which cytokine from macrophages and dendritic cells drives Th1 differentiation?
IL-12.
Which Th2 cytokine causes B cells to switch to IgE?
IL-4 (IL-13 also contributes).
Which subset is deficient in hyper-IgE syndrome with STAT3 mutation, and what infections follow?
Th17 cells; patients have recurrent staphylococcal skin abscesses and chronic mucocutaneous candidiasis.
Which transcription factor defines regulatory T cells?
FOXP3; its mutation causes IPEX syndrome.
Related
- T-cell activation: two signals and superantigens
- B-cell activation, class switching and affinity maturation
- Granulomatous inflammation
- Antibody structure and isotypes (IgG, IgA, IgM, IgE, IgD)
- CD4⁺ helper T cell
- Regulatory T cell (Treg, FOXP3)
- Cytokines: the table to know
- Interferon-γ
- IL-4, IL-5 and IL-13 (the Th2 cytokines)
- Interleukin-17
- IL-12 and IL-23
- IL-10 and TGF-β (the brakes)
- Type I hypersensitivity (immediate, IgE)
- Type IV hypersensitivity (delayed, T cells)
Related conditions
Microorganisms
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: 21.3 The Adaptive Immune Response: T lymphocytes and Their Functional Types (OpenStax (Anatomy and Physiology 2e), 2022); 18.3 T Lymphocytes and Cellular Immunity (OpenStax (Microbiology), 2016).
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Representative model, for educational purposes only.