Eczema and Asthma Share a Link. Can it Lead to New Treatments?

On the surface, asthma and eczema may not seem related — but two UC San Francisco researchers are collaborating in ways that could uncover new treatments based on underlying connections.

The collaboration is between two biomedical researchers, Mark Ansel, PhD, and Marlys Fassett, MD, PhD, who seem to come from different worlds.

Ansel is a UCSF professor of microbiology and immunology who studies how different molecules guide the development and behavior of immune cells, with a focus on why lungs become inflamed during asthma attacks.

Fassett is a dermatologist at UCSF Health who treats patients’ itchy allergic reactions, like eczema, in the clinic. She’s also a UCSF professor who studies the biology of eczema and related skin conditions.

But their chance connection two decades ago has blossomed into a collaboration that bridges the laboratory and clinic to advance the science of itch, allergy and asthma. Such collaborations are central to UCSF’s pursuit of better therapies for patients — and they’re already producing results.

“Our clinicians always want to do better for their patients, but they’re also really interested in how disease works and they know that’s the key to finding new ways to treat their patients,” Ansel said. “That’s part of the magic of this place.”

Why is eczema so itchy?

In 2012, Fassett arrived at UCSF to pursue her dermatology residency, armed with a joint MD-PhD degree from Harvard University and the Massachusetts Institute of Technology. One of the worst symptoms of eczema her patients experience is incessant itch, spurring them to scratch their sore skin and make things worse.

Fassett was curious about an immune protein known as the “itch cytokine” that had been previously discovered by other scientists. It was no surprise that it was abundant in the skin of her patients with eczema, but it wasn’t clear what the protein was doing or how to get it under control.

There has to be interchange between clinicians and basic scientists to move the needle.”

Ansel, who had mentored Fassett for three months in the early 2000s at Harvard, hadn’t worked on the itch cytokine himself, but was familiar with similar immune proteins from his work on asthma. The itch cytokine and those asthma-related molecules were made by the same type of immune cell, the T-cell.

“These T-cells were in his scientific wheelhouse,” Fassett says. “I already knew I could be very honest with Mark about both my excitement for the science and when things weren’t working, which is actually a good thing in research.”

Ansel invited Fassett to join his Parnassus research building lab, and Fassett began to split her time between itch experiments and attending to her patients.

Synergy from bench to bedside

It wasn’t long before Fassett and Ansel’s research began to point to common mechanisms in many allergic and immunologic disorders, eczema and asthma among them.

“With asthma, there’s an underlying, allergy-like immunity, driven by T-cells,” says Ansel, chair of the UCSF Bakar ImmunoX Initiative, the campus hub for immunology. “One new drug, dupilumab, which targets several immune molecules in the lungs, has transformed care for many allergic-asthma patients and even some with COPD. Those same molecules are also in skin, and Marlys and her dermatology colleagues prescribe them to help people with eczema.”

The itch cytokine remains the focus of both scientists, even as Fassett has left Ansel’s laboratory to start her own research group. Together and independently, they’re looking into other drugs that target the immune system, including nemolizumab — now in clinical trials for eczema — that might also treat asthma and other diseases.

“Immunology has had a big impact on cancer and many other diseases, even psychiatric diseases, in the last decade or two, but we still have a lot of work to do,” Ansel says. “The real impactful insights keep coming from the community working together. There has to be interchange between clinicians and basic scientists to move the needle.”