Want to live a long and healthy life? We're exploring the science behind chronic inflammation and how it contributes to early-onset disease.
Research led by Dr Raffi Gugasyan shows how certain key biomarkers, called ‘cytokines’, can accelerate ageing and what we can do about it.
Inflammation is a natural process the immune system uses to protect the body from infections and injuries.
However, persistent or chronic inflammation, known as ‘inflammageing’, can damage healthy tissues, accelerate ageing, and increase susceptibility to conditions such as heart disease, kidney dysfunction, liver complications and neurological decline.
People with multiple chronic conditions, such as diabetes or cardiovascular disease, tend to have elevated markers of systemic inflammation. That’s why understanding and addressing these changes in the immune system is essential to improving the quality of life in our later years.
Dr Raffi Gugasyan explains ‘inflammageing’: the process of low-grade inflammation that accumulates as we age.
Dr Raffi Gugasyan speaks: ‘Inflammageing’ is the process of low-grade inflammation that accumulates as we age.
A by-product of inflammageing is the accumulation of an unusual B cell called age-associated B cells, which are quite prominent in the elderly. However, the production of age-associated B cells is rapidly accelerated in immunocompromised individuals - patients with primary immunodeficiency, for instance, or individuals with autoimmune disease or cancer.
What we understand is that the frequency of age-associated B cells is higher in females than males and this is best reflected in disease severity being quite prominent in females.
It's currently unknown what triggers the development of age-associated B cells, but our preliminary evidence indicates that a soluble factor called the cytokine is responsible for triggering the development of age associated B cells, which in turn secrete factors contributing to multi-organ immune-mediated damage.
In this study, we plan to identify the responsible cytokine and use cytokine-specific antibody-mediated therapy that will diminish the cytokine levels, reduce the production of age-associated B cells, and ultimately attenuate chronic inflammatory-mediated disease. Thank you. End of transcript.
Dr Raffi Gugasyan and his team are investigating the cellular triggers of inflammation.
The research focuses on immune cells known as B cells, which play a critical role in protecting the body against infections.
In healthy individuals, the immune system maintains a good balance of these cells. But as we age—or in individuals with chronic disease conditions such as HIV, cancer, or hepatitis C—this balance shifts. There are fewer naïve B cells and a growing number of age-associated B cells, increasing the risk of inflammation-related organ damage.
Raffi and his team have recently identified new biomarkers (biological signals that help track immune system changes) that may be driving unnecessary inflammation in older adults. These findings, though not yet published, represent a major step forward in our understanding of age-related immune decline.
“We are looking at this cellular activity and inflammation that leads to vulnerability to early onset illness,” says Raffi.
“Our goal is to slow or even prevent that decline.”
By pinpointing the transitions between naïve and aged-associated B cells, the team is exploring therapeutic strategies to moderate inflammation. This could involve developing new drugs or repurposing existing medications to maintain immune balance and preserve organ function.
Raffi and his team have recently identified new biomarkers (biological signals that help track immune system changes) that may be driving unnecessary inflammation in older adults. These findings, though not yet published, represent a major step forward in our understanding of age-related immune decline.
“We are looking at this cellular activity and inflammation that leads to vulnerability to early onset illness,” says Raffi.
“Our goal is to slow or even prevent that decline.”
By pinpointing the transitions between naïve and aged-associated B cells, the team is exploring therapeutic strategies to moderate inflammation. This could involve developing new drugs or repurposing existing medications to maintain immune balance and preserve organ function.