The immune system is the body's main defence system against infections or other foreign substances.
When a virus, or other invading body attacks a cell, the cell sends out a chemical as a warning signal. This initially alerts white blood cells called macrophages. When macrophages encounter the invader they encircle and digest it.
Macrophages are also called antigen presenting cells (APC), because once some of the invading bugs have been destroyed by the initial immune response, particles of the debris, called antigens, are carried by these cells to another type of white blood cell called T-lymphocytes or T-cells.
There are different types of T-cells. The ones involved in this process are called helper T-cells. The helper T-cells respond to the antigen and orchestrate the appropriate response to the invader by encouraging the production of a range of molecules that tell other elements in the immune system how to respond. These molecules include interferons. At the start of an immune response, messenger molecules are released that stimulate a wide range of cells including other white blood cells such as B-lymphocytes, or B-cells, and killer T-cells (also known as cytotoxic T-cells). One of these messengers is gamma interferon.
B-cells are tuned to specific invaders. When the invader is found in the body, the B-cell clones itself and produces millions of antibodies. Antibodies are proteins that lock onto the surface of the invading particle helping the body to kill it off.
Killer T-cells kill the body's own cells that have been invaded, preventing the germ from reproducing and then infecting other cells.
The immune response causes inflammation of the damaged or infected tissue. Inflammation causes local blood vessels to dilate, increasing blood flow to the injured site and allowing more white blood cells to attack invaders in the affected area.
Once the infection is under control, helper T-cells release different messenger molecules including beta interferon that help to calm down the immune response.
Last updated: 3 June 2013
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