Understanding ‘inflammageing': the process of inflammation and ageing
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.
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.
The Journal of Experimental Medicine
Elisha de Valle, Jasper K.S. Cornish, Raffi Gugasyan, Jasper K.S. Cornish, Elisha de Valle, Raffi Gugasyan, Elisha de Valle, Jasper K.S. Cornish, Raffi Gugasyan
The EMBO Journal
Elisha Horat, Raffi Gugasyan, George Grigoriadis, Meredith O’Keeffe, Raelene J. Grumont, Ashish Banerjee, Steve Gerondakis, Raffi Gugasyan, Elisha Horat, George Grigoriadis
Cancer Cell
Elisha de Valle, Raffi Gugasyan, Elisha de Valle, Raffi Gugasyan
Science Translational Medicine
Elisha de Valle, Raffi Gugasyan, Elisha de Valle, Raffi Gugasyan
Frontiers in Cellular and Infection Microbiology
Joshua A. Hayward, David Jose Delgado-Diaz, David Tyssen, Raffi Gugasyan, Anna C. Hearps, Gilda Tachedjian, David Jose Delgado-Diaz, David Tyssen, Joshua A. Hayward, Raffi Gugasyan
Mucosal Immunology
Raffi Gugasyan, Anna C. Hearps, David Tyssen, Daniela Srbinovski, David Jose Delgado-Diaz, Muriel Aldunate, Gilda Tachedjian, Anna C. Hearps, David Tyssen, Daniela Srbinovski
Immunity
Raffi Gugasyan