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For more information, go to www.arthritisresearchuk.org

Professor Rizgar Mageed

Professor Rizgar MageedProfessor Rizgar Mageed is professor of experimental immunology at Queen Mary University of London.

What does your work involve?

As an academic, I divide my time between research, teaching and administrative duties. Research takes most of my time; I lead a research team with interest in understanding why the immune system goes wrong in patients with rheumatic diseases. We aim to identify new targets for which we can develop targeted therapies. Our main focus is on B-lymphocytes, which are key immune cells that protect from infections. We hope to be able to identify disease-causing cells and target them for therapy.

How long has Arthritis Research UK been funding you?

I have been very fortunate and equally grateful that Arthritis Research UK has funded my research for over 25 years. Arthritis Research UK, then known as Arthritis and Rheumatism Council, funded my first research project at the University of Birmingham with my mentor Professor Roy Jefferis on studying the structure of a type of antibodies to self-proteins called rheumatoid factors. These studies led to a range of collaboration with international groups and gave me a platform on which to build my career.

What’s the most important thing you have found out in the past 12 months? And why?

There are two areas where we have made what we think are important observations. First, a collaborative study with Professor David Isenberg that is funded by Arthritis Research UK on B-lymphocytes in patients with lupus have identified subsets of B-lymphocytes which we believe directly contribute to the disease process. We have been able to gain insights into how the regulation of such cells goes wrong in lupus and how they could contribute to the disease process. Second, we have observed that patients with rheumatoid arthritis can be stratified based on the main mechanism that drives their chronic inflammatory responses. This observation also helped us to start to explain why some patients respond favourably to treatment with biologic anti-tumour necrosis factor alpha (TNFα) agents while others do not. Patients from the latter group appear to have excess of a T-lymphocytes subset, known as T-helper 17 lymphocytes (Th17) that produce interleukin 17, which is not inhibited by biologic anti-TNFα agents. We hope that both observations will help us make our aims of developing new treatment strategies achievable.

What do you hope or expect to achieve as a result of your Arthritis Research UK funding?

We hope that we can confirm and extend our observations on identifying immune cells that promote pathology in lupus and arthritis. We are hopeful that such confirmation will not only provide some new insights into the diversity of disease mechanisms in different patient groups but also leads to the development of more specific therapies with fewer side-effects.

What do you do in a typical day?

On regular days, I have meetings with my colleagues and students to discuss progress in their studies and design new experiments. I am also involved in teaching immunology to our medical students. I also spend a significant part of my time in writing papers and grant applications.

What is your greatest research achievement?

I consider all verifiable research discoveries to be important as even what we perceive to be small could provide bedrocks for better understanding and progress. For me, perhaps, my early studies on the structure and genetics of rheumatoid factor production in patients with rheumatoid arthritis have given me new perspectives on disease mechanisms. These studies led me to explore the nature of lymphocyte abnormalities in patients more closely.

Why did you choose to do this work?

I was fortunate to be introduced to autoimmunity by my first mentor, Professor John Holborow, who was one of the pioneers of the field. His knowledge, enthusiasm and human qualities initiated my strong desire to learn more about immunology and understand why rheumatoid factors are produced and why patients develop autoimmunity.

Do you ever think about how your work can help people with arthritis?

This is something I think about all the time. It is a privilege work in the field I work in and to have access to clinical samples from the wonderful patients that give their consent for our studies, and I am always conscious that I should do all I can to justify their trust and generosity.

What would you do if you weren’t a clinician/researcher?

I would have liked to be a professional sportsman.

About Rizgar

In addition to reading, mostly about history, and classical music, I am a fan of all sports.

This article first appeared in Arthritis Today Winter 2014, issue 163.
For more information, go to www.arthritisresearchuk.org.
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