T-helper subset pathways in autoimmune disease (Th1, Th2, Th17)
Core concept
| Th1 | Th2 | Th17 | Treg | Tfh | |
|---|---|---|---|---|---|
| Induced by | IL-12 (+ IFN-gamma) | IL-4 | IL-6 + TGF-beta; maintained by IL-23** | TGF-beta + IL-2 | IL-6, IL-21 |
| Transcription factor | T-bet | GATA3 | RORgammat | FOXP3 | Bcl-6 |
| Signature cytokines | IFN-gamma, IL-2, TNF | IL-4, IL-5, IL-13 (+IL-6, IL-10) | IL-17A/F, IL-22, GM-CSF | IL-10, TGF-beta | IL-21 |
| Effector arm | Macrophage activation, CD8 help, IgG1/IgG3 opsonising antibody | Eosinophils (IL-5), IgE class switch (IL-4/IL-13), mucus, mast cells | Neutrophil recruitment (via IL-8/G-CSF), antimicrobial peptides and defensins (IL-22) | Suppression, tolerance | Germinal centre B-cell help |
| Defends against | Intracellular - mycobacteria, Listeria, Salmonella, viruses, fungi | Helminths | Extracellular bacteria and fungi - Candida, Staphylococcus at mucosal surfaces | - | All |
| Disease when excessive | Sarcoid, TB granuloma, T1DM, Crohn's, Hashimoto | Asthma, atopic dermatitis, allergic rhinitis, EGPA, ABPA | Psoriasis, PsA, axSpA, MS, RA, Crohn's | Immune deficiency if excessive (tumour) | Autoantibody disease |
- Th1 and Th2 are mutually inhibitory - IFN-gamma suppresses Th2, IL-4 suppresses Th1
- Th17 and Treg share a differentiation branch - TGF-beta alone -> Treg; TGF-beta + IL-6 -> Th17; inflammation flips the switch
- The subsets are plastic, not fixed - Th17 can convert toward Th1 in chronic inflammation
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