Basic immunology for beginners

Since the 1950s, scientists had known the basic outline of how the body protects itself from disease-causing microbes (pathogens) through its immune system. As a result of the work of Sir Macfarlane Burnet at the Walter and Eliza Hall Institute in Melbourne, it was clear that the cells of the immune system could recognise what was the body's own material (called 'self') and distinguish it from what was foreign (non-self). The immune system always assumes that non-self material is dangerous and attacks it. Most invading germs are therefore wiped out. (In 1960, Burnet was a joint winner of the Nobel prize for his contribution to immunology.)

When Peter Doherty arrived in Canberra in 1972 to start his post-doctoral work, research had shown that the immune system uses different mechanisms to deal with the various types of invaders it is likely to face. One part of the system (the B-cells) produces antibodies, which are protein molecules designed to latch on to foreign biochemicals. This part of the system is often called humoral immunity or antibody-mediated immunity. Any substance that causes antibodies to be made is termed an antigen. The attachment of antibodies to antigen molecules on the outside of a pathogen can have various effects. It may, depending on which antigens are affected, stop the functioning of the pathogen entirely. But it can also make the pathogen more likely to be destroyed by another 'arm' of the immune system – the microbe-eaters.

White blood cells called phagocytes can crawl around the body and literally eat up material that is signalled as ripe for destruction. (This eating is called phagocytosis.) A coating of antibodies around a pathogen can be one way of encouraging phagocytosis.

Another part of the immune system is responsible for dealing with the rather different set of problems posed by viruses. Viruses are much smaller than bacteria and multiply inside our own cells. To eliminate them, the body needs to identify and kill virus-infected cells before they release a deadly cargo of new viruses. A type of white cell known as the T cell is able to do this. As a result it's called a killer (or cytotoxic) T-cell. (Other types of T-cell have different functions, including regulating B cells. The whole T-cell part of the system is called cellular or cell-mediated immunity.)

But why should natural-born killer cells go into action against the body's own cells – surely they are seen as self? Fortunately for the immune system, most viruses cause the cells they are infecting to carry virus antigens on their surface. For example, if a virus is inside the cells lining the back of your throat, some of the virus antigens get put onto the outside of those cells; your immune system will think these cells are foreign and destroy them. A layer of cells is killed, and so your throat feels sore. (But don't worry, the cell layer is quickly replaced.) In many infectious diseases, most of the damage is actually done by our own immune systems. In their all-out attempts to defeat pathogens, they cause heavy 'civilian casualties' and a fair amount of 'collateral damage' – but we usually win the war in the end.

Another feature of the immune system has been known for a long time: transplanted organs are attacked by the very body that they are grafted into – this is the phenomenon of rejection that is a major problem in modern surgery. It's not universal in biology - you can do grafting and transplanting in plants and lower animals, but mammals and birds have a system to detect transplants as foreign and reject them. This is based on the fact that each individual has a collection of their own unique antigens on their own cells and these antigens differ from those of others. Thus, although heart cells from any human have many antigens in common, your heart cells will also have your own individual antigenic signature that's different from mine. This collection of highly individually variable antigens is called the major histocompatibility complex (MHC) in mammals, but Human Leucocyte Antigen in humans. 'Tissue-typing' before transplant surgery tries to match up as many of these individual antigens as possible between the donor and the recipient.

But it wasn't clear to biologists why a system should have evolved that expends effort to identify cells from another member of the same species as foreign. Transplants don't happen in nature, so why bother evolving these MHC antigens and plastering all our cells with them as a sort of trademark?

Doherty and Zinkernagel came up with a sensible answer to this question, as well as finding out more about what controls the killer T-cells. The two scientists brought together the work on MHC antigens with that being carried out on the response to virus infections.

November 1996

Back to top

© Academy homepage | Education | Academy contacts | Search