WITH all the usual coughs and colds around at this time of year, it is fortunate that we can generally rely on our immune system to protect us from their potentially devastating effects.
Luckily, the human immune system is a highly evolved fighting machine, having honed its skills against the relentless onslaught of killer microbes such as smallpox, which plagued our ancestors.
Now it contains a veritable arsenal of lethal weap
ons that can be called into action the moment a foreign microbe is spotted. White blood cells are the mainstay of the defence, as they patrol the body looking for trouble. Once an invader is identified there is a good chance it will be rapidly engulfed, killed and digested by amoeba-like cells called polymorphs and macrophages.
These cells also produce chemical signals called cytokines that attract the attention of lymphocytes and give them a kick start. They divide rapidly to produce an army of millions of cells; T lymphocytes that kill microbes or microbe-infected cells directly, and B lymphocytes that produce antibodies to neutralise the attacker.
But all this immune activity inside our bodies often induces nasty side- effects. In fact, the typical symptoms of fever, headache, sore throat, tender glands and general feebleness we experience with flu, for example, are mostly caused not by the invading microbe itself, but by the immune response generated to fight it. Indeed, in certain cases, like glandular fever and viral hepatitis, an over-enthusiastic immune response may do serious damage to vital organs.
What controls the army of immune cells hell-bent on fighting invaders, and how is the battle brought to an end?
Obviously, there must be some mechanism within our highly sophisticated immune system for preventing unwanted damage and recognising when the battle is won. But exactly what this is has puzzled scientists for decades. Recently, however, a new type of T lymphocyte has been discovered called a regulatory T cell, or Treg.
Tregs provide a counter- balance to the active fighting T cells, calming them down by producing cytokines that defuse their killing mechanisms and stop them dividing. They ensure that once the invader is conquered the whole episode fades into memory, but the troops can still be mustered quickly if the same microbe attacks again.
Over the past few years, research on Tregs has been intense and we now know their effects go far beyond the control of immunity to microbes. Even when we are healthy they play a vital role in persuading our immune cells to spare our body's own cells from attack, a situation that can cause autoimmune diseases such as insulin-dependent diabetes and rheumatoid arthritis if Treg control is lacking.
Scientists have also turned their attention to looking at how pregnant mothers remain healthy when we know that white cells from the baby pass through the placenta into the mother's body. Since a baby only shares half its mother's DNA, there are plenty of "foreign" molecules on the baby's cells to tempt the mother's immune systems to attack them. Fortunately this does not happen, and again it is the Tregs that come to the rescue by preventing her fighting T cells from responding.
More recently, scientists from the University of California in San Francisco have shown that cells from a pregnant mother also regularly cross the placenta into the developing foetus, with up to 0.8 per cent of cells in the baby's lymph organs being of maternal origin.
It was assumed these "foreign" cells are tolerated because the baby's immune system is too immature to respond to them, but the scientists now show it is down to Tregs yet again.
Surprisingly, these regulatory cells develop very readily in the foetus, and in some cases they could still be found up to 17 years later. This may be a mixed blessing – on the one hand the researchers speculate that the propensity for a foetus to generate Tregs could help when a severely anaemic baby needs an intrauterine blood transfusion by preventing an immune reaction, but on the other hand the long-lived Tregs may damp down a child's response to vaccines later in life.
• Dorothy H Crawford is professor of medical microbiology at Edinburgh University.
