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Dr Simon Kollnberger

Simon KollnbergerDr Simon Kollnberger is an Arthritis Research UK non-clinical career development fellow at the MRC human immunology unit at the University of Oxford.

What does your work involve?

I'm working as an Arthritis Research UK-funded career development fellow with Dr Paul Bowness in Oxford, researching the immunology of seronegative spondyloarthropathy. Collectively these are the third most common types of arthritis in the UK (after osteoarthritis and rheumatoid arthritis) and include ankylosing spondylitis, reactive arthritispsoriatic arthritis and juvenile spondyloarthropathy. These conditions have a very strong association with possession of the HLA-B27 gene. Our lab has been investigating the reasons for this association.

HLA-B27 is a member of an important group of proteins found on the surface of immune cells that are involved in the body’s defence against bacteria and viruses. In an infection, these proteins bind fragments of virus or bacteria inside the cell and display them on the cell surface where they can then be recognised by immune cells. In addition, these proteins bind groups of molecules/receptors on the surface of cells that ensure that an individual’s immune response is switched on and off at the appropriate time.

We're studying how a novel form of B27 called B272 may be involved in arthritis. We think that infection stimulates B272 production. B272 binds receptors on immune cells that may stop the immune response from being switched off. We find greater numbers of immune cells with a receptor that binds B272 in patients. We're investigating how these cells damage cells in the joints and how B272 binding to receptors on these cells allows this damage to continue unchecked.

How long has Arthritis Research UK been funding you?

Arthritis Research UK has funded me since 1999, first as a post-doctoral scientist and subsequently since 2003 as a non-clinical career development research fellow.

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

In the last year, in collaboration with a Swiss research group, we've made antibodies which recognise B272. This is an exciting development because it'll greatly help our studies into what affects B272 production in patients and how binding to receptors influences disease.

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

We hope to find out how B272 binding to immune receptors influences the course of spondyloarthropathy. This improved understanding may help the development of treatments to prevent disease, especially if we can develop antibodies that block the stimulating effect of B272 on inflammation in arthritis.

What do you do in a typical day?

The majority of my time at the moment is spent working in the lab but I'm starting to spend an increased proportion teaching and training students and writing grants. Designing experiments requires a lot of forward planning so a significant amount of my time is spent reading about what people have done before and then applying this information to what I want to do. Later, we present our results at meetings around the world and in publications.

What's your greatest research achievement?

Probably the most important discovery I've made is showing that the new form of B27 we've discovered, B272, binds differently to immune receptors from B27. Subsequently, working with Dr Toni Chan and Dr Paul Bowness, we showed that immune cells with receptors for B272 are found in increased numbers in patients with B27-associated arthritis.

Why did you choose to do this work?

I think research chose me rather than the other way round. I enjoy the whole creative process of having an idea, putting it into action and taking it through to a successful conclusion. The really great thing about working in a laboratory is the variety of jobs you get to do, so there's never a dull moment and you're always learning something new.

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

Yes, very much so. Practically, in the long-term, our work could lead to the development of therapeutic antibodies, which, by blocking B272 binding to immune cells, may lead to improved treatment. More immediately, improved understanding of the causes of disease could lead to better ways of preventing arthritis. A very important part of all this is communicating new findings to patients.

What would you do if you weren’t a scientist?

I enjoy science so much I can't really imagine doing anything else. I get the same creative buzz from doing art, so I guess, if I could, I'd be an artist.

About Simon

My wife and I live in a beautiful part of Oxfordshire, which is fantastic for walking. Apart from this most of my free time is divided between art, playing the piano, gardening and long-distance running.

This article first appeared in Arthritis Today Summer 2007, issue 137.

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