Introduction
The body's first line of defence is its collection of non-specific defences, including phagocytes such as macrophages. If these are overwhelmed, activation of the powerful immune system follows. Immunity possesses three key attributes not seen with non-specific defences:
- Specificity
- Memory
- Tolerance
Specificity Unlike mechanism such as inflammatory response and the phagocytic action of macrophages, which are triggered by a wide range of threats, an immune response is directed against one antigen and no other
Memory Again, unlike general defence mechanisms, an immune response against a particular antigen will usually generate immunological memory of the antigen. This means that the immune response on subsequent exposures to the same antigen is generally faster and more powerful.
Tolerance he cells of the immune system are aggressive and potentially extremely destructive. Control of their activity is essential for protection of healthy body tissues. As immune cells travels around the body, they check the markup proteins that cells show on their cell membranes. Heathy body cells display the expected ' self' markers and are ignored by the trolling immune cells. However, non-self cells, such as cancer cells, foreign cells or pathogens, possess different patterns of markers, which immediately activate the immune cell and usually lead to the destruction of the non-self cell.
Lymphocytes
Lymphocytes make up 20-3-% of circulating white blood cells but at any one time most of them are found in lymphocytic and other tissues rather then in the blood stream.
They include natural killer cells involved in immunological surveillance, T-cells and B-cells. T-cells and B-cells are responsible for immunity and are produced in the bone marrow and some lymphatic tissues, although T-cells migrate to the thymus gland for final maturation.
For each of the millions of possible antigen that might be encountered in life, there is a corresponding T-and B-cell programmed to respond to it. There are, therefore, vast numbers of different T- and B-cells in the body, each capable of responding to only one antigen
T-cells
The hormone thymosin, produced by the thymus gland, is responsible for promoting T-cell maturation, which leads to the formation of fully specialised, mature, functional T-cells. It is important to recognise that a mature T-cell has been programmed to recognise only one type of antigen and during its subsequent travels through the body will react to no other antigen, however dangerous it might be. Thus, a T-cell manufactured to recognise the chickenpox virus will not react to a measles virus, a cancer cell, or a tuberculosis bacterium.
B-cells
These are produced and matured in the bone marrow. They produced antibodies, proteins designed to bind to, and destroy, an antigen. As with T-cells, each B-cell targets one specific antigen; the antibody released reacts with one type of antigen and no other. B-cells provide antibody-mediated immunity.
Cell- mediated immunity
T-cells that have matured in the thymus gland are released into the circulation.when they encounter their antigen for the first time, they become sensitised to it. If the antigen has come from outside of the body, it needs to be 'presented' to the T-cell on the surface of an antigen-presenting cell. There are different type of antigen-presenting cell, including macrophages. Macrophages are part of the non0specific defences, because they engulf and digest antigens indiscriminately, but they are a crucial link cell between initial non-specific defences and the immune system. After digesting the antigen they transport the most antigenic fragment to their own cell membrane and display it on their surface. They display this antigen to the T-cell that has been processed to target that particular antigen, activating the T-cell.
If the antigen is an abnormal body cell, such as a cancer cell, it too will be displaying foreign material on its cell membrane that will stimulate the T-cell. Whichever way the antigen is presented to the T-cell, it stimulates it to divide and proliferate. Four main type of specialised T-cell are produced, each of which is still directed against the original antigen, but which will tackle it in different ways.
Cytotoxic T-cells
These directly inactivate any cells carrying antigen. They attach themselves to the target cell and release powerful toxins, which are very effective because the two cells are so close together. The main role of cytotoxic T-cells is in destruction of abnormal cells, e.g. infected cells and cancer cells.
Helper T-cells
Helper T-cells These are essential not only for cell-mediated immunity, but also antibody-mediated immunity. Their central role in immunity is emphasised in situations where they are destroyed, as by the human immunodeficiency virus (HIV).
T-helper are the most commonest of the T-cells; their main functions include:- production of chemicals called cytokines, e.g. interleukins and interferons, which support and promote cytotoxic T-cells and macrophages.
- Cooperating with B-cells to produce antibodies; although B-cell are responsible for antibody manufacture, they require to be stimulated by a helper T-cell first.
Suppressor T-cells
These cells acts as 'brakes', turning off activated T- and B-cells. This limits the powerful and potentially damaging effects of the immune response. Suppresser T-cells are also thought to help prevent the development of auto-immunity and to protect the fetus in pregnancy.
Memory T-cells
These long lived cells survive after the threat has been neutralised, and provide cell-mediated immunity by responding rapidly to another encounter with the same antigen.
Antibody-mediated (humoral) immunity
B-cells are much less mobile than T-cells, and spend much of their time in lymphoid tissue, e.g. the spleen and lymph nodes. B-cells, unlike T-cells, recognise and bind antigen particles without having to be presented with them by an antigen-presenting cell. Once its antigen has been detected and bound, and with the help of an activated helper T-cell, the B-cell enlarge and begins to divide. It produces two functionally distinct types of cel, plasma cell and memory B-cells.
Plasma cells
These secrete massive quantities of antibodies into blood. Antibodies are carried throughout the tissues. Plasma cells live no longer than a day and produce millions of molecules of only one type of antibody, which targets the specific antigen that originally bound to the B-cells. Antibodies:
- bind to antigen, labelling them as targets for other defence cells such as cytotoxic T-cells and macrophages
- Bind to bacterial toxins, neutralising them
- Activate complement
Memory B-cells
Like memory T-cells, these cells remain in the body long after the initial episodes has been deals with, and rapidly respond to another encounter with the same antigen by stimulating the productions of antibody-secreting plasma cells.
The fact that the body does not normally develop immunity to its own cells is due to the fine balance that exist between the immune reaction and its suppression. Autoimmune disease are due to the disturbance of this balance.
Acquired immunity
The immune response to an antigen following the first exposure is called the primary response. Second and subsequent exposures give rise to a secondary response.
The primary response Exposure of the immune system to an antigen for the first time leads to a slow and delayed rise in antibody levels, peaking 1-2 weeks after infection. This delayed response reflects the time required to activate the T-cells system, which then stimulates B-cells division. Antibody level start to fall once the infection is cleared, but if the immune system has responded well, it will have generated a population of long-lived memory B-cells, making the individual immune to future infections.
The seconadry response subsequent exposures to the same antigen, the immune response is much faster and 10-15 times more powerful, because the memory B-cells generated after the first infection rapidly divide and antibody production begins almost immediately.
Active naturally acquired immunity
The body may be stimulated to produce its own antibodies by:
Having the disease During the course of the illness, B-cells develop into plasma cells that produce antibodies in sufficient quantities to overcome the infection. After recovery, the memory B-cells produced confer immunity to future infection by the same antigen.
Having a subclinical infection Sometimes the infection is not sufficiently severe to cause clinical disease but stimulates sufficient memory B-cells to establish immunity, e.g. hepatitis A, in other cases , subclinical infection may be too mild to stimulate an adequate response for immunity to develop.
Active artificially acquired immunity
This type of immunity develops in response to the administration of dead or live artificially weakened pathogens or deactivated toxins. The vaccines and toxoids retain the antigenic properties that stimulate the development of immunity but they cannot cause the disease. Many infectious disease can be prevented by artificial immunisation.
Active immunisation against some infectious disorders gives lifelong immunity, e.g. diphtheria, wooing cough or mumps. In other infections the immunity may last for a number of years or for only a few weeks before revaccination is necessary.
Passive naturally acquired immunity
This type of immunity is acquired before birth by the passage of maternal antibodies across the placenta to the fetus, and to the baby in breadth milk. The variant of different antibodies provided depends on the mother's active immunity. The baby's lymphocytes are not stimulated and this form of immunity is short lived.
Passive artificially acquired immunity
In thus type, ready-made antibodies, in human or animal serum, are injected into the recipient. The source of the antibodies may be an individual who has recovered from the infection, or animals, commonly horses, that have been artificially actively immunised. Specific immunoglobulins may be administrated prophylactically to prevent the development of disease in people who have been exposed to the infection, e.g. rabies, or therapeutically after the disease has developed.
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