[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [Immunology](https://durgical.com/en/immunology/) › [Cytokines and molecules](https://durgical.com/en/immunology/#a-molecules) › IL-4, IL-5 and IL-13 (the Th2 cytokines) [Immunology](https://durgical.com/en/immunology/) · [Cytokines and molecules](https://durgical.com/en/immunology/#a-molecules) # IL-4, IL-5 and IL-13 (the Th2 cytokines) - Molecule IL-4, IL-5 and IL-13 run allergic (type 2) inflammation: IgE, eosinophils and mucus. They are targets of modern asthma and eczema biologics. Updated 2026-11-01 ## Key points - IL-4: Th2 differentiation and IgE class switch in B cells. - IL-5: eosinophil maturation, release from marrow and survival. - IL-13: goblet-cell mucus, airway hyperreactivity, remodelling; raises exhaled nitric oxide (FeNO). - IL-4 and IL-13 share the IL-4 receptor α chain: dupilumab blocks both. - Biomarkers of type 2-high asthma: blood eosinophils, FeNO, total IgE. - Anti-IL-5 (mepolizumab), anti-IL-5Rα (benralizumab), anti-IL-13 (tralokinumab), anti-IgE (omalizumab). ## What it is IL-4, IL-5 and IL-13 are the signature cytokines of type 2 immunity, made by Th2 cells and by group 2 innate lymphoid cells (ILC2). Epithelial alarm signals (TSLP, IL-33, IL-25) start the response after allergen contact. Together they produce IgE, recruit and sustain eosinophils and remodel the airway, which defines type 2-high asthma and atopic disease. ## Function - Defence against helminths (worms) is the physiological role of type 2 immunity. - IL-4 inhibits Th1 responses, and IFN-γ inhibits Th2: the two arms balance each other. - IL-4 induces adhesion molecules (VCAM-1) that help eosinophils leave the blood. ## Step by step - Allergen contacts the airway epithelium, which releases TSLP, IL-33 and IL-25. - Dendritic cells and ILC2 respond; naive CD4 T cells become Th2 cells under IL-4. - IL-4 (with IL-13) switches allergen-specific B cells to IgE; IgE binds FcεRI on mast cells. - IL-5 expands eosinophils, which enter the airway wall and release granule proteins. - IL-13 causes mucus, smooth-muscle hyperreactivity and fibrosis: chronic asthma. ## Clinical notes - Allergic and eosinophilic asthma, allergic rhinitis, chronic rhinosinusitis with nasal polyps. - Atopic dermatitis: dupilumab and IL-13 blockers (tralokinumab, lebrikizumab). - Eosinophilic esophagitis and hypereosinophilic syndromes (dupilumab, mepolizumab, depending on the condition). - Biologics do not treat an acute asthma attack; they reduce exacerbations and oral steroid needs. ## In the lab - Blood eosinophil count and total serum IgE. - Fractional exhaled nitric oxide (FeNO) as a marker of IL-13 activity in the airway. ## Memory aid Four builds the IgE, five feeds the eosinophils, thirteen floods the airway with mucus. ## Test yourself Think of the answer, then tap the question to see it. ## Which cytokine is essential for eosinophil development and survival? IL-5; mepolizumab blocks IL-5 and benralizumab blocks its receptor. ## Why does dupilumab block both IL-4 and IL-13? It binds the IL-4 receptor α chain, which is part of the receptors used by both cytokines. ## Which three markers point to type 2-high asthma? Raised blood eosinophils, raised fractional exhaled nitric oxide and raised total IgE. ## What is the normal (non-allergic) role of type 2 immunity? Defence against helminths and tissue repair; allergy is the same response aimed at harmless antigens. [Add to my cards (4)](https://durgical.app/estudiar/?add=/en/immunology/il-4-il-5-and-il-13/) ## Related - [Cytokines: the table to know](https://durgical.com/en/immunology/cytokines-the-table-to-know/) - [Fc receptors, BCR and TCR](https://durgical.com/en/immunology/fc-receptors-bcr-and-tcr/) - [Interferon-γ](https://durgical.com/en/immunology/interferon/) - [Th1, Th2, Th17, Tfh and Treg](https://durgical.com/en/immunology/th1-th2-th17-tfh-and-treg/) - [Eosinophil](https://durgical.com/en/immunology/eosinophil/) - [Mast cell and basophil](https://durgical.com/en/immunology/mast-cell-and-basophil/) - [Type I hypersensitivity (immediate, IgE)](https://durgical.com/en/immunology/type-i-hypersensitivity/) - [Monoclonal antibodies and biologics: naming and targets](https://durgical.com/en/immunology/monoclonal-antibodies-and-biologics-naming-and-targets/) ## Related conditions - [Asthma](https://durgical.com/en/conditions/asthma/) - [Allergic rhinitis](https://durgical.com/en/conditions/allergic-rhinitis/) - [Anaphylaxis](https://durgical.com/en/conditions/anaphylaxis/) [← All of immunology](https://durgical.com/en/immunology/) 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: [T-helper cells and their cytokines in pathogenesis and treatment of asthma](https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2023.1149203/full) (Frontiers in Immunology, 2023); [Immunologic aspects of asthma: from molecular mechanisms to disease pathophysiology and clinical translation](https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1478624/full) (Frontiers in Immunology, 2024); [Tralokinumab-ldrm injection: MedlinePlus Drug Information](https://medlineplus.gov/druginfo/meds/a622011.html) (MedlinePlus (U.S. National Library of Medicine), 2025); [Pro-Inflammatory and Anti-Inflammatory Interleukins in Infectious Diseases: A Comprehensive Review](https://pmc.ncbi.nlm.nih.gov/articles/PMC10818686/) (Tropical Medicine and Infectious Disease (PubMed Central), 2024). ## **Spotted a mistake?** We are always improving for the community. Tell us what is wrong and our team will review it. Report a mistake Representative model, for educational purposes only. --- Source: https://durgical.com/en/immunology/il-4-il-5-and-il-13/ License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/immunology/il-4-il-5-and-il-13/