How immune complexes affect the blood vessels depends very much on what sort of antibodies they contain – there are five different isotypes. In the healthy person, the main antibody formed to food is immunoglobulin A, or IgA, which has special protective properties. Unlike most other antibodies it does not activate the defensive proteins in the blood known as the complement system.
The products of the complement system cause inflammation, a reaction designed to mobilize the body’s protective forces. The effects of inflammation are to make the blood vessels in the vicinity more leaky and to attract other immune cells into the area – the leaky vessels make it easier for the immune cells to gain access to the surrounding tissues. What appears on the outside as a swollen, red, tender area is in fact a microscopic battleground, where the body’s own cells and tissues are unfortunate casualties of the general mayhem.
The purpose of inflammation, in the healthy individual, is to fight off infection. The body assumes that the antibodies have attached themselves to an invading bacterium or virus and sends in the troops. Obviously the body needs to have control systems that tell it not to react when the antibodies are bound to something innocuous – such as a food protein which happens to have wandered into the blood through the gut wall. This is the function of IgA. Because it does not activate the complement system it can quietly mop up non-harmful antigens for disposal by the phagocytes, without setting off a damaging episode of inflammation.
For this system to work, the body must somehow distinguish food from other sorts of antigen. And it must make sure that IgA – rather than IgG, another more inflammatory type of antibody – is manufactured to fit the food molecules. The details of how the body does this are still far from clear, but a general picture is emerging from current research, and this is described in Chapter Twelve. The process is known as ‘the induction of oral tolerance’.
What, if anything, goes wrong with this system? There is only a limited amount of evidence available, but it does seem that the system for producing IgA rather than IgG to food molecules breaks down in some people. Where this occurs, the immune complexes circulating in the blood after a meal will be potentially inflammatory. If they are deposited in a blood vessel, damage to the walls of the vessel will follow.
Such people may also have IgE in their food-molecule immune complexes, so mast cells could be triggered to add to the inflammation. Whether this actually happens is not clear. But if it does then there are important implications for the way we think about allergies: the dividing line between Type I (IgE) food allergy and Type III food allergy may not be as sharp as is often assumed.
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