Written by Aisha Saleem, Pharmacist & Health Writer at PharmaHealths.com
Last Updated: July 2026
When patients ask me why Dupixent works for eczema but not psoriasis, or why Cosentyx works for psoriasis but not eczema, the answer comes down to four specific cytokines: IL-4, IL-13, IL-17, and IL-23. These are the molecular messengers at the heart of both conditions, and understanding what each one does makes the logic of modern biologic therapy immediately clear. Each biologic drug is essentially a highly targeted blocker of one or two of these signals, which is why the right drug depends entirely on which condition and which cytokine pathway is driving the disease in a given patient.
Quick Summary for Busy Readers
• IL-4 and IL-13 drive eczema
• IL-17 and IL-23 drive psoriasis
• Dupilumab blocks IL-4 and IL-13 together
• IL-17 inhibitors act quickly on psoriasis plaques
• IL-23 inhibitors work upstream and may give longer lasting control
What Are Cytokines and Why Do They Drive Skin Disease?
Cytokines are small signaling proteins produced by immune cells that coordinate the immune response by carrying instructions between cells. In healthy skin, cytokines help manage responses to infection, injury, and environmental triggers before resolving once the threat has passed. In chronic skin diseases like psoriasis and eczema, specific cytokines become chronically overproduced, locking the immune system into a self-sustaining inflammatory cycle that cannot resolve on its own.
According to the National Institute of Allergy and Infectious Diseases, the cytokine environment in a skin lesion determines what type of inflammation is happening, which cells are recruited, how quickly skin cells proliferate, and whether the barrier is disrupted or intact. This is why identifying which cytokines are dominant in a given condition is not just scientifically interesting: it directly determines which biologic drug will work and which will have no effect.
A simple way to think about cytokines is as messages between immune cells. In eczema and psoriasis, the wrong messages keep getting repeated, which is why inflammation does not switch off naturally. Biologic treatments work by blocking specific messages at the source.
What Is IL-4 and What Does It Do in Eczema?
IL-4 is a cytokine produced primarily by Th2 immune cells, mast cells, and basophils, and it is one of the two dominant drivers of atopic dermatitis. IL-4 signals through a receptor complex called the IL-4 receptor alpha subunit, and its effects on the skin are significant: it suppresses the production of filaggrin and other proteins essential to the skin barrier, promotes the differentiation of more Th2 cells, and drives IgE production from B cells, the class of antibody central to allergic responses.
Research published in the Journal of Allergy and Clinical Immunology has established that IL-4 is elevated in both the skin and blood of patients with active atopic dermatitis, and that it contributes to both the skin barrier disruption and the systemic Th2 immune skewing that makes eczema patients more susceptible to asthma, hay fever, and food allergies as part of the atopic march.
What Is IL-13 and How Does It Differ From IL-4 in Eczema?
IL-13 is closely related to IL-4 and shares part of its receptor complex, the IL-4 receptor alpha subunit, which is why blocking this shared receptor with dupilumab interrupts both cytokines simultaneously. IL-13 drives skin barrier impairment, mucus production in the airways relevant to asthma, and itch signaling through a direct effect on sensory nerve fibers. According to the British Journal of Dermatology, IL-13 is the cytokine most directly linked to the intense itch experienced by atopic dermatitis patients, which is why treatments targeting the IL-4 and IL-13 pathway reduce itch scores so significantly in clinical trials alongside improving visible skin inflammation.
The practical reason Dupixent blocks both IL-4 and IL-13 through a single injection is precisely because they share this receptor subunit. By binding the IL-4 receptor alpha subunit, dupilumab prevents both cytokines from signaling simultaneously, which is clinically more effective than blocking either one alone.
Many patients notice that itch improves first when this pathway is blocked, even before the skin fully clears, which reflects how strongly IL-13 is linked to itch signaling.
What Is IL-17 and What Does It Do in Psoriasis?
IL-17A is the primary effector cytokine in psoriasis and one of the most important therapeutic targets in modern dermatology. It is produced mainly by Th17 cells, a subset of T lymphocytes, and by mast cells, gamma-delta T cells, and innate lymphoid cells in lesional skin. Research published in Frontiers in Immunology has established that IL-17A acts directly on keratinocytes, driving them to proliferate rapidly and produce large quantities of pro inflammatory chemokines and antimicrobial peptides that recruit further immune cells to the skin, amplifying and sustaining the psoriatic plaque.
IL-17A also has effects beyond the skin: it acts on neutrophils, endothelial cells, fibroblasts, and in the joint, on osteoclasts and chondrocytes, which is why elevated IL-17 is relevant to both the skin plaques and the joint inflammation of psoriatic arthritis. IL-17 inhibitors like secukinumab and ixekizumab bind directly to IL-17A and neutralize it, preventing it from reaching its receptor on keratinocytes and other cells and interrupting the inflammatory cascade at a direct effector level.
One important practical consideration with IL-17 inhibition is that IL-17 also plays a role in defending against certain fungal organisms, which is why IL-17 inhibitors are associated with an increased rate of mucocutaneous candidiasis, a recognized side effect noted across the clinical trials for both Cosentyx and Taltz as reviewed by the Journal of the American Academy of Dermatology.
In clinical practice, IL-17 inhibitors are often chosen when rapid skin clearance is a priority, as they tend to work faster than upstream treatments.
What Is IL-23 and How Does It Relate to IL-17?
IL-23 sits upstream of IL-17 in the same inflammatory pathway and is produced primarily by dendritic cells and macrophages in response to triggers including infections, skin injury, and stress. Its key function in psoriasis is to activate and sustain Th17 cells, the immune cell subset responsible for producing IL-17A. Without IL-23, Th17 cells cannot be maintained in their activated state, which means that blocking IL-23 shuts down the source of IL-17 production rather than just neutralizing IL-17 after it has been released.
According to research published in the New England Journal of Medicine on IL-23 inhibitors including risankizumab, this upstream positioning is one reason IL-23 inhibitors produce particularly durable responses, with some patients maintaining near complete skin clearance even after stretching or pausing treatment. By targeting the signal that sustains the inflammatory cycle at its source, IL-23 inhibitors may allow the underlying immune dysregulation to settle more durably than blocking IL-17 directly, though both approaches are highly effective and the clinical choice between them depends on individual patient factors.
This is why IL-23 inhibitors are often preferred when long-term disease control and less frequent dosing are important considerations.
What Is the IL-23/IL-17 Axis and Why Does It Matter for Treatment?
The IL-23/IL-17 axis is the term used to describe the upstream-downstream relationship between IL-23 and IL-17 in psoriasis. IL-23 is the upstream activator, IL-17 is the downstream effector, and the axis between them is the central inflammatory highway in psoriatic disease.
Research published in Frontiers in Immunology has characterized this axis as the most therapeutically important pathway in moderate to severe psoriasis, with drugs targeting either end of it consistently outperforming older treatments like methotrexate and TNF inhibitors in clinical trial head-to-head data.
Understanding the axis also explains a clinically important practical point: IL-17 inhibitors tend to have a faster onset of action, since they neutralize the effector cytokine directly, while IL-23 inhibitors may produce more durable long-term responses because they work at a deeper regulatory level. Neither is categorically superior, and both represent major advances over older systemic psoriasis treatments.
What Is the Difference Between Eczema and Psoriasis Cytokines?
• Eczema is driven by IL-4 and IL-13, leading to barrier damage and itch
• Psoriasis is driven by IL-17 and IL-23, leading to rapid skin turnover and plaques
Why Do Eczema and Psoriasis Require Different Cytokine Targets?
Eczema and psoriasis look similar on the skin but are driven by fundamentally different cytokine environments, which is precisely why they require different targeted treatments. Eczema is a Th2-dominant condition driven by IL-4 and IL-13, while psoriasis is a Th17-dominant condition driven by IL-17 and IL-23. Using a drug that blocks IL-17 in eczema has no meaningful effect because IL-17 is not the primary driver of atopic dermatitis. Using dupilumab in psoriasis similarly produces no psoriasis specific benefit because the IL-4 and IL-13 pathway is not the dominant inflammatory mechanism in plaque psoriasis.
This cytokine-based distinction is what makes getting the correct diagnosis so important before starting any biologic treatment, and it illustrates why dermatologists now think in terms of cytokine pathways rather than just visible symptoms when selecting treatments for moderate to severe skin disease.
The Bottom Line
IL-4 and IL-13 are the cytokine drivers of eczema, blocked by dupilumab through their shared receptor. IL-17 and IL-23 are the cytokine drivers of psoriasis, blocked respectively by IL-17 inhibitors like Cosentyx and Taltz, and by IL-23 inhibitors like Skyrizi. Understanding what each cytokine does, and why each drug targets the ones it does, is what turns a confusing list of biologic options into a logical map of precisely targeted treatments. If you’re being treated for psoriasis or eczema with a biologic, knowing which cytokine your medication targets help you understand what it’s doing in your body and what to expect.
Before starting treatment, it is always worth asking which cytokine pathway your therapy targets and how quickly you can expect to see improvement, as this helps set realistic expectations and improves treatment confidence.
FAQs
Q1: What does IL-17 do in psoriasis?
IL-17A is the primary effector cytokine in psoriasis, produced by Th17 immune cells and acting on keratinocytes to drive rapid skin cell proliferation and sustained inflammation. It recruits further immune cells to the skin and sustains the inflammatory plaque cycle. IL-17 inhibitors like secukinumab (Cosentyx) and ixekizumab (Taltz) neutralize IL-17A directly to interrupt this process.
Q2: What is the IL-23/IL-17 axis?
The IL-23/IL-17 axis describes the upstream-downstream relationship between two key cytokines in psoriasis. IL-23 activates and sustains Th17 cells, which produce IL-17A, the primary effector cytokine driving skin inflammation. IL-23 inhibitors like Skyrizi block the axis upstream while IL-17 inhibitors like Cosentyx block it downstream, with both approaches highly effective for moderate to severe psoriasis.
Q3: How does Dupixent block IL-4 and IL-13?
Dupixent (dupilumab) blocks the IL-4 receptor alpha subunit, which is shared by both IL-4 and IL-13 as part of their receptor complex. By blocking this one shared subunit, dupilumab prevents both cytokines from signaling simultaneously, which is why a single injection targeting one receptor produces therapeutic effects on both IL-4 and IL-13 driven inflammation in atopic dermatitis.
Q4: What is the difference between IL-17 and IL-23 inhibitors for psoriasis?
IL-17 inhibitors like Cosentyx and Taltz neutralize IL-17A directly at the effector level, producing a faster onset of action. IL-23 inhibitors like Skyrizi block IL-23 upstream, shutting down the source that produces and sustains IL-17A, and tend to produce more durable long-term responses. Both classes are highly effective for moderate to severe psoriasis, with the choice depending on individual patient factors and treatment goals.
Q5: What are the cytokines in eczema vs psoriasis?
Eczema is driven primarily by the Th2 cytokines IL-4 and IL-13, which disrupt the skin barrier and drive the allergic-type immune response. Psoriasis is driven primarily by the Th17 cytokines IL-17 and IL-23, which drive rapid skin cell proliferation and sustained plaque formation. These fundamentally different cytokine environments explain why eczema and psoriasis require different biologic treatments.
Q6: Does blocking IL-17 affect the immune system’s ability to fight infections?
Yes, IL-17 plays a role in the body’s natural defense against certain fungal organisms, which is why IL-17 inhibitors are associated with an increased risk of mucocutaneous candidiasis, mild fungal infections of the skin or mouth. This risk is recognized and manageable, and standard antifungal treatment is effective, but patients starting IL-17 inhibitors should be aware of the connection and report any unusual fungal symptoms early.
Q7: Why does blocking IL-23 work better upstream than blocking IL-17?
Blocking IL-23 upstream shuts down the signal that activates and sustains Th17 cells, the primary producers of IL-17A. This means fewer IL-17 molecules are produced in the first place, rather than simply neutralizing IL-17 after release. Research published in the New England Journal of Medicine on IL-23 inhibitors suggests this deeper regulatory level of intervention may contribute to the more durable skin clearance responses seen with drugs like risankizumab compared to some IL-17 inhibitors.
Q8: Which cytokines are shared between eczema and psoriasis?
IL-13 and IL-22 are produced in both conditions, though at different levels and with different dominant roles. IL-17 and IL-22 are both elevated in psoriasis and to a lesser degree in chronic eczema, though IL-17 inhibitors are not effective for eczema because the overall cytokine environment and immune driver are fundamentally different between the two diseases.
Call to Action
If this article helped you understand the cytokines behind your skin condition, I have dedicated guides covering how each of these pathways is targeted by individual biologic drugs on PharmaHealths.com, including full breakdowns of Dupixent for eczema, and Cosentyx, Skyrizi, and Taltz for psoriasis. Head over to PharmaHealths.com to explore the full biologics series and build a complete picture of how targeted immune therapy works for your condition.
Disclaimer
This article is for general informational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. Always consult your doctor, dermatologist, or pharmacist before starting, stopping, or changing any treatment.
References
• National Institute of Allergy and Infectious Diseases
• Journal of Allergy and Clinical Immunology
• British Journal of Dermatology
• Frontiers in Immunology
• Journal of the American Academy of Dermatology
• New England Journal of Medicine