Inflammation is something that we all experience. When we get injured, it causes redness around a cut. When we’re fighting an infection, inflammation is important for creating the defenses that trap and kill pathogens. In small doses, inflammation is a good thing because it protects us and starts the healing process.
But what happens when inflammation doesn’t turn off?
Imagine a fire alarm goes off to alert of nearby smoke and sets off a sprinkler. This response is an important warning and stops the danger. Now, imagine if the alarm and sprinkler don’t stop. This creates irritating noise and a big mess that needs to be cleaned up. That’s what can happen with inflammation. When the immune system stays activated for too long, it can damage healthy tissues and organs and contribute to serious diseases.
My lab’s research is asking a fundamental question: Why does inflammation sometimes fail to resolve, and can we teach the body to finish the job?
We study autoimmune disease, conditions that affect millions of people, where the immune system mistakenly attacks the body’s own healthy cells. Today’s treatments work by suppressing the immune system. They can provide tremendous relief, but there’s an important trade-off: immune suppression leaves patients more vulnerable to infections and cause serious side effects. Many patients also see their disease return when treatment stops.
My research team is exploring a different approach to treat autoimmune inflammation. Instead of turning down the immune response, what if we could both calm the immune system and activate the body’s natural mechanisms for resolving inflammation?
We are using animal models of autoimmune bone marrow failure, a serious disease where they body cannot make enough blood cells. We’ve found evidence that the body’s normal inflammation-resolution processes are impaired in autoimmune disease. We’re now developing combination treatments designed to address both sides of the problem: controlling harmful immune activity while helping the body actively resolve inflammation.
Our early results in animal models are encouraging. Combining these approaches improves efficacy, produced more lasting responses, and reduced treatment-related toxicity.
There’s still work to do before these findings can be translated into treatments for people. But our goal is to develop therapies that work better, are safer, and may allow patients to spend less time on medications that suppress their immune systems.
And that vision is moving beyond the laboratory.
Kate MacNamara is professor in the Department of Immunology and Microbial Disease at Albany Medical College. She leads a research program investigating how inflammation impacts the bone marrow, the site of blood production. MacNamara co-founded a startup company called Resolvia Biosciences with Rachel Grazda, a postdoctoral researcher and lead research scientist on the project.
Empire State Development announced Resolvia Biosciences as a finalist for the annual Commercialization Competition, which will take place Oct. 27 and 28, 2026, at the Buffalo Convention Center during the New York State Innovation Summit.
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