Run that past me again...
Reproduced from Issue 105 of Arthritis Today
Professor Brian Henderson of University College is fed up with the inability of science to communicate to the man or woman in the street. In the first of a series of articles, he attempts to de-mystify the scientific jargon surrounding much arthritis research.
What is he talking about? How many times have you said this when listening to some "expert" on radio or TV?
We live in a world which is awash with new discoveries in science, medicine and technology. This brings with it a bewildering variety of new concepts, each with its own words, abbreviations and acronyms. Even scientists, who deal with this world on a daily basis, find it difficult to follow fields of scientific research outside their own area of interest.
Therefore, how much more difficult is it for the proverbial person in the street, who has no scientific training, to follow the twists and turns of scientific debate and discussion.
Fortunately, it is now being recognised that "he who pays the piper calls the tune". Although grant applications are written for an expert panel of scientists and therefore can be very complex, the major research funding agencies, be they government (Medical Research Council) or charitable (arc) are now asking applicants to provide a lay summary so that they can be understood by the vast majority of people who have no scientific training.
The UK's largest scientific funding agency, the Wellcome Trust, has launched a competition, with a prize of £25,000, to enable the winner to write a book on their research which will "educate, captivate and inspire the non-specialist lay-reader."
arc, on its part, is producing a series of articles on the charity's research funding which attempts to unravel its technical complexities. In this first article, the chosen topic is cytokines.
Cytokines – friend or foe?
The human body is an unbelievably complex piece of biological engineering with an enormous number of parts – called cells. These cells form the organs and tissues of our bodies, and to function properly they must communicate with each other.
The advances made in communication over the past few hundred years (semaphore, telegraph, telephone, e-mail) are paralleled by advances in understanding of biological communication. In the 18th century Galvani discovered the first form of biological communication – nerve conduction. It was only at the turn of the 19th century that the second form of biological communication, which uses endrocrine hormones, was discovered.
Endocrine hormones are produced by specialised glands in our bodies, and are released into the bloodstream in which they circulate to reach their target tissues.
Throughout the course of our life, our body's normal functions are controlled by hormones and by our nervous system. From time to time, outside agents such as bacteria and viruses invade our body and cause disease. Under such conditions our nervous systems and hormones are of limited use.
Fortunately, we have an "elite force" of molecules – proteins called cytokines, which have only been discovered during the past few decades. These molecules have a major role in controlling our immune system in its battle to repel invading bacteria and viruses, repel the invaders, and drive them from the body's borders.
Normally, having completed their task, the cytokines disappear. However, in autoimmune diseases such as rheumatoid arthritis – one of the most common chronic inflammatory diseases – they fail to disappear and stay around attacking the body, particularly the joints, causing pain and damage.
Much of current understanding of cytokines has come from the work of clinicians and scientists studying rheumatoid arthritis. There are well over 100 cytokines and Professor Tiny Maini and his team at the Kennedy Institute in London have spent a number of years tracking down one cytokine which we now believe is principally responsible for the symptoms of rheumatoid arthritis.
Everyone has the ability to produce this cytokine, which is known as tumour necrosis factor – abbreviated to TNF. It can kill tumour cells but is probably more important in dealing with infectious agents. For most of us, TNF is a real friend, performing its role and then diappearing.
Unfortunately, for people with rheumatoid arthritis, TNF is a foe, because of it fails to disappear and keeps on being produced.
There has been a tremendous amount of research into ways to making the cytokines go away (switching off, in scientific parlance), or blocking their activity. A number of different methods have reached the stage of being tried in patients with inflammatory diseases.
The Kennedy Institute has been testing an antibody called cA2 which binds to TNF and stops it working. This has proved to be effective and may become available in the UK in 1999 as a product called called Remicade. Like all drugs, stopping the treatment allows the symptoms of the disease to return.
Another way of blocking TNF is to use a natural protein present on our cells. Such a formulation has recently received approval in the USA and should be available in the UK as the drug Enbrel, also during 1999.
Both these therapies offer only temporary relief, and are only effective as long as the drug continues to be administered. It is not yet known if anti-TNF therapies also prevent the destruction of the joints which occur in the disease.
TNF can also be blocked by a drug from the past – thalidomide – famous for causing birth defects. This drug is being used for treating an arthritic disease called Behcet's syndrome in which patients suffer joint symptoms along with ulcers (eg in the mouth) and eye inflammation.
It should not be thought that TNF is the only cytokine involved in the many arthritic diseases that the Arthritis Research Campaign is interested in. Research is going on to find out more about this elite force of cytokines and their roles in the different forms of arthritis disease. A key question is – what controls their appearance and disappearance? If we understand the answer to this key question we may be able to switch cytokines on and off as well, and in consequence, control all forms of arthritis disease.
However, in order to understand more about the workings of cytokines, we need to know about the cells involved in controlling immunity. These cells and their role in inflammation and disease will be described in other articles in this series.
