Our bodies are protected by a number of devices:

The skin made mainly of a protein called keratin, which is highly resistant to bacterial and fungal attack, acts as a barrier to restrict entry into the delicate internal tissues. There are a number of sites which cannot be protected by skin and these have alternative mechanisms to restrict bacterial and viral entry.

Lysozyme: This is an enzyme secreted into the tears, into the mucous lining the gut and the respiratory tract. It acts upon a substance called murein which makes up the cell wall structure of bacteria. Some bacteria, the gram negative types, have a lipid covering on the murein outer wall to resist damage from the lysozyme.

Mucous and cilia: The nasal cavities and the trachea, bronchus and bronchioles are covered by a ciliated epithelium. The cilia are small hair like extensions of the exposed cell membranes and they contain contractile protein fibrils arranged as an outer ring of 9, with 2 central fibrils. When ATP is supplied the proteins react to cause a stiff bending at the base of each cilium, and these then relax and move back into an upright position in a curving action which creates no backflow. We therefore get a power stroke and a recovery stroke from each cilium. The contractions and relaxations of the cilia are coordinated so that metachronal waves run from the base of the lungs towards the glottis at the top of the larynx. In the nasal cavities tha wave runs from the nostrils towards the back of the pharynx. These wave actions push the mucous secreted from the golgi apparatus of epithelial cells in a constant stream out of the lungs and nasal passages to the top of the oesophagus where the mucous is swallowed. Bacterial and viral particles breathed into the system are trapped in this mucous and hopefully are moved out and swallowed into the acid stomach before they can invade our cells. The acid conditions of the stomach are largely there to act as a sterilisation mechanism since the vast majority of bacteria cannot live in acid conditions.

Blood Clotting: When the skin is damaged the blood vessels in the dermis are torn and the damaged cells release histamine. This activates the thrombocytes, or platelets to initiate the blood clotting mechanism. The histamine also causes dilation of capillaries in the surrounding area, which reduces the speed at which the blood flows and makes it easier for phagocytic lymphocytes attracted by the histamine to leave the capillaries by moving through the gaps between the cells in the capillary walls. The clotting mechanism is extremely complex requiring at least thirteen different factors. It can be simplified as follows:

The clot is formed from long sticky threads of fibrin proteins formed from the globular fibrinogen found in the plasma of the blood. The thrombin enzymically converts fibrinogen to fibrin. The thrombin is itself formed from a precursor found in the plasma called prothrombin and this can only happen if the platelets, or damaged cells release thromboplastin and if the necessary clotting factors are present in the plasma. The threads of fibrinogen form a network over the wound and trap red blood cells to form the clot which then dries to seal the wound. Beneath the scab, the tissues will regenerate. To prevent the clotting reaction from running out of control and affecting distant tissues which are undameged there is an anticlotting agent, Anti-thromboplastin found in the plasma which deactivates thromboplastin if it is carried into the circulatory system. When the wounds are extensive secondary thrombosis can occur due to movement of thromboplastin in blood vessels to distant sites.

Bacteria which enter the blood stream are usually attacked by phagocytic white cells and ingested and digested by them. However some bacteria especially those with mucilage coats can evade detection by the white cells and then spread to cause disease symptoms. Some bacteria may enter the lymph fluids and again it is possible for them move around the body and therefore a defence is needed. The lymph glands are situated at vital points throughout the lymph system and these contain huge numbers of lymphocytes and these will restrict the further movement of the bacteria if they are recognised. 

There are two main components to the human immune system, the cell-mediated response and the humoral response. The cell mediated response deals mainly with cellular defects, such as virus infected cells, cancer cells and in modern times transplanted cells. The humoral resonse deals with antibody production to defend us from infective organisms, especially bacteria. Some terms need to be clearly understood before we deal with these defence mechanisms:

ANTIGEN - a molecule usually of a complex type, often a protein or glycoprotein (a protein with a carbohydrate chain added to it). Any molecule which can trigger antibody production is an antigen. An antigen must be recognisable as ‘non-self’, you must remember that our own cells are covered with complex molecules which must not trigger our defence mechanism or we would destroy our own structure. This does happen in what are known as autoimmune diseases such as Multiple Sclerosis where the myelin sheaths of nerve cells are attacked and destroyed with the result that the control of muscle activity is progressively lost.

ANTIBODY - a molecule produced and released into the blood stream which will bind with a particular antigen. All antibodies have the same basic structure. They can be visualised as two heavy protein chains hinged so that they bend into a Y-shape and connected by a disulphide bond. To the splayed arms are attached light chains, held in place by disulphide bonds. The tips of the Y-shaped arms are variable in structure while the remainder of the molecule is of constant construction. It is the amino acid groupings on the variable ends which allow the antibody molecule to attach to the antigen by attraction to the chemical groups on the antigen molecule.

LYMPHOCYTE- a white blood cell. There are many different types which stain differently and they have different nuclear shapes and this gives them their technical names. However we are only interested in their functional names and the main types are:

b-lymphocytes: These cells secrete antibodies into the blood plasma, tissue fluid and lymph once they are activated. They can be divided into two forms. Effector cells, which are actively secreting antibodies. Memory cells which are inactive or dormant cells ready to be activated should the need arise.

T cells: These get their name from the fact that they are activated by the thymus gland, which lies in the chest cavity just over the heart.

T4 or T-helper cells: These cells are instrumental in activating the b-lymphocytes to become effector cells.

T8 Cells: There are two types of these, one group acts as Killer or Cytotoxic cells used in the cell-mediated response. The other group of T8 cells are the Suppressor cells, these cells can switch off the production of antibodies by restricting the cloning of b-lymphocytes.

INTERLEUKINS: Also called lymphokines, these are chemical released by T cells which can activate or inhibit cloning of b-lymohocytes and convert memory cells into active effector cells.

A phagocytic cell known as a macrophage attacks and digests a micro-organism. The structural molecules in it are broken into discrete sections called epitopes. Each epitope is displayed on the macrophages surface.

T-helper cells, each with their own distinct antigen recognition molecule on their surface will contact the macrophage and if the epitope and recognition molecules match a reaction occurs and interleukin I is released. This activates the T-helper cell to secrete interleukin II onto any b-lymphocyte it meets which carries the same antibody type as its recognition molecule.

InterleukinII will cause the b-lymphocyte to undergo a rapid series of mitotic cell divisions, cloning itself to form a large population of lymphocytes all producing the same antibody type.

The action of the antibodies when they react with the antigen bearing microorganism can cause a range of actions, agglutination may result because of the exposed antibody tails reacting with other bondined antidody tails so that they stick together. The bacteria will be clumped into groups and this limits their ability to spread through the tissues and makes it easier for them to be caught and engulfed by the phagocytes. The commonest form of action is for the antibody to act as an ‘EAT ME’ marker. The phagocytes have a recognition molecule on their surface which will bind to the exposed tails of any attached antibodies.

The important point to note about the humoral response is that once an antigen has been identified by our system we develop a huge reserve of memory cells capable of producing antibodies against it. This makes for efficient use of resources. We only develop the ability to produce antibodies in large quantities if the antigen exists in our environment. The memory cells will enable us to produce a fast and massive response to any later attack by the infectious organsism so that disease symptoms rarely appear twice. Of course if the organism modifies its antigen then we become susceptible to attack again!

If a human cell is displaying antigens which are of a non-self type then the cytotoxic T8 cells will attack it and destroy it. This is useful in the defence of the body against cancer and viral infection. If the viral infected cell can be recognised and destroyed we can prevent its replication and spread, there are mechanisms in the cell to cause the display of abnormal antigens on the cell membranes as soon as the virus invades the cell. Many but not all types of cancer cells can be destroyed in this way too. The various T8 cells carry antigen recognition molecules on their surfaces to enable them to detect the foreign antigens being displayed by the damaged or infected cells. Unfortunately these cells cannot react to a transplant which carries foreign antigen signatures in any other way than to kill it. Thus immunosuppressant drugs are needed in transplant surgery where there is any difference in the cell markers.

The potential T- cells pass through the thymus gland just after birth and they travel past macrophage cells which are displaying our own antigens. If a T-cell reacts with one of these self antigens it is killed by the macrophage.

If the T-cell is carrying a recognition molecule which does not react with any of our own displayed antigens, then it is allowed to survive and becomes part of our defence system.

Antibody Release:

When an antigen is first contacted the antibody produced is called an IgM, for immunoglobulin type M. This is secreted in a relatively small amount and deals with the initial infection (hopefully!). We refer to this as the primary response. If the antigen is met on a second occasion then both IGM and a second type called IgG is released. Both of these have the same variable antibody endings but the heavy protein chains making up the backbone of the antibody are slightly different. The IgG is produced in much larger quantities and this will produced for a number of months or even years. This secondary response is quick enough and powerful enough to prevent the disease organism from taking hold in the body and therefore we are unaware that we have been infected again. You can see why a number of vaccination methods require a booster phase every so often!