Immunology Unlocked: How Cytokines, Cells, and Targeted Therapies Shape Modern Dermatology

At Dermatology Week APP Day 2025, Douglas DiRuggiero, DMSc, MHS, PA-C, delivered a dynamic session titled “Immunology Review for Common Dermatoses”—a high-energy crash course connecting textbook immunology to real-world therapeutics. In his signature conversational style, DiRuggiero guided attendees through the inner workings of the immune system and explained how modern dermatologic drugs act like “snipers,” targeting the cellular culprits of chronic skin disease.

“If you’ve ever wondered why IL-4, IL-13, JAK1, and TNF alpha show up in so many treatment labels, this talk explained exactly why,” he said.

Kicking off with the basics, DiRuggiero revisited the split between the innate and adaptive immune systems. The innate side? Fast but nonspecific—think of it as the SEAL team on standby. The adaptive side? Slower, but smarter and equipped with B cells, which produce antibodies, and T cells, which mediate inflammation and memory.

“The B in B cells,” he explained, “actually comes from a bursa in a chicken’s butt. I’m not kidding.”

From there, he walked through the development of plasma cells, antibodies (immunoglobulins), and how different T-cell types emerge depending on which cytokine messages they receive.

When exposed to IL-12, a T-cell becomes TH1. With IL-4, it becomes TH2. With IL-23, TH17. These T-helper subtypes go on to drive chronic diseases like psoriasis, eczema, and alopecia areata—each with their own cytokine “fingerprints.”

DiRuggiero’s point was clear: When you understand the immunologic roadmap, modern dermatology drugs make perfect sense.

“If the message can’t get through the window, the cell won’t misbehave.”

He broke down where different drugs act:

• Monoclonal antibodies (the -mabs) block cytokines or their receptors outside the cell.
•  Small molecule inhibitors (the -nibs) work inside the cell, blocking enzymes like Janus kinases (JAKs) from transmitting inflammatory signals.

He showed how this plays out in practice. For example, in alopecia areata, IL-15 and interferon gamma stimulate cytotoxic T cells to attack the hair follicle. But if you block JAK1, JAK2, or JAK3, you can interrupt that loop and allow regrowth, explaining the rationale behind newer JAK inhibitors now approved for hair loss.

In diseases like atopic dermatitis, IL-4 and IL-13 are the troublemakers, whereas psoriasis is driven by IL-17 and IL-23. Drugs like dupilumab, risankizumab, and secukinumab make sense when you understand which cells and cytokines they target.

To lighten the load, DiRuggiero layered in visual aids, real-world analogies, and memorable one-liners: “Janus kinase was named after the Roman god with two faces. But if you ask me, they should’ve called them mullet kinases—business in the front, party in the back.”

More than just a science lesson, this session armed APPs with a deeper understanding of the diseases they treat every day and the targeted therapeutics revolutionizing outcomes.

“If you’ve grasped these pathways,” DiRuggiero said, “then I now deputize you as a cutaneous immunologist.”

For more meeting coverage, visit the Dermatology Week APP Day newsroom.

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Reference

DiRuggiero D. Immunology review for common dermatosis. Presented at: Dermatology Week; October 22–25, 2025; Virtual.