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Shir Sun Raffi Gugasyan

Diagnostic Markers in Chronic Immune Disorders

Understanding ‘inflammageing': the process of inflammation and ageing

About

Our group focuses on understanding the process of inflammageing and how certain inflammatory pathways promote the development of unusual B cells (‘age-associated B cells'). We explore how certain factors or cytokines contribute to accelerated immune-mediated ageing in individuals living with chronic diseases, such as primary immunodeficiencies and autoimmune disease.

Our research is based on the use of pre-clinical models that reflect on human conditions of chronic immune-mediated disease.

Our major objective is to identify and characterise critical immunological targets, such as cytokines, that are responsible for the process of immune-mediated ageing in: 

  • the elderly, and 

  • patients living with primary immunodeficiencies, autoimmunity or cancer. 

We validate our findings in human systems. We then progress through Burnet’s Commercialisation team and collaborating industry partners. The overall rationale is to develop critical immunological targets that can be considered for existing therapeutic antibodies or for the development of novel therapies. 

Watch our video on inflammageing

Associate Professor Raffi Gugasyan discusses 'inflammageing', the process of low-grade inflammation that accumulates as we age. 

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.

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Dr Raffi Gugasyan

Dr Raffi Gugasyan

Chair of Education; Head, Diagnostic Markers and Chronic Immune Disorders
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Group members

Dr Raffi Gugasyan

Dr Raffi Gugasyan

Chair of Education; Head, Diagnostic Markers and Chronic Immune Disorders
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Shir Sun

Shir Sun

PhD Candidate
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