The term ‘early arthritis’ as we currently know it is really a misnomer, according to an international expert in immunology.

Speaking at this year’s ARA annual scientific conference Scotland’s very own Professor Iain McInnes told delegates that as long as patients had damaged bone they did not have ‘early arthritis’.

“Early arthritis is a result of immunologic decisions that happen in minutes and hours, long before a patient becomes aware that they have arthritis,” he said, noting that in a perfect world, early arthritis clinics should really be seeing patients ten years before they get signs and symptoms of disease.

This was because the sequence of events that ultimately become inflammation in the joints, start up to several years before a patient walks through the door of an arthritis clinic saying they are tired, miserable and their joints ache, said Professor McInnes in a talk called the immune system in motion.

The immune system is regulated by different pathways at the early stages of an immune response as opposed to the later stages, he explained.

However there was a tendency for clinicians to ignore this fundamental truth and to treat patients with therapies across the range of disease duration clinical presentations with a single targeted agent, and yet to expect them to get better regardless of the stage of disease or of the immune system at each of those sequential time points.

“It’s a miracle that we even see 60 percent modest response rates and absolutely predictable that we can only get in the order of 20 to 25 percent of patients doing really well with any one given intervention,” he told delegates.

The immune system can’t wait

The immune system is akin to a catapult held in tension and it cannot wait. Patients typically have a level of immunological upset that can go on for months, even years, before the joint becomes involved.

The Holy Grail would be to get to a point where we could treat people with a pre-form of rheumatoid arthritis, however as Professor McInnes acknowledges, this is no easy task.

“We’re going to have to first of all find such at risk people and that’s a science in itself,” Professor McInnes told the limbic.

“How do you find these people in the population – how do you screen for these abnormalities?” he asked.

“Then once you’ve found them you have to understand the immunological events that are going on during pre-RA phase when the immune system is disturbed but hasn’t yet attacked the joint” he added.

 “We don’t really have the answer to that yet – it’s a work in progress,” he said.

 Using mouse models to understand current treatments

 Professor McInnes and his team based at Glasgow University in Scotland have been using mouse models to get a window on the very early events that occur in the immune system that allow it to switch itself on and make the decision to damage musculoskeletal tissues.

In particular McInnes and his team have looked at the impact some selected current therapies have on the way the immune system, particularly lymphocytes and dendritic cells, are switched on.

Under the influence of some effective therapies, they discovered cells were switched on in an abnormal way – in that they refuse to become activated.

“What this drug actually does is it allows lymphocytes to see their target but instead of being switched on and becoming aggressive and damaging the joint they’re switched on into a state of ignorance and they no longer engage with their target and cause damage,” he said.

“At one level these models allow us to look at how current therapies work but in terms of applying that to the future of how we might treat pre-RA status, it’s too early” he added. “But we are optimistic!”