Good day everyone, Today we are going to discuss fully on immunity;
After studying this section, you should be able to:
- discuss the roles of the different types of T-lymphocyte in providing cell-mediated immunity
- describe the process of antibody-mediated immunity
- distinguish between artificially and naturally acquired immunity, giving examples of each
- distinguish between active and passive immunity, giving examples of each.
The body’s first line of defence is its collection of non- specific defences, including phagocytes such as macro- phages. If these are overwhelmed, activation of the powerful immune system follows. Immunity possesses three key attributes not seen with non-specific defences: specificity, memory and tolerance.
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Specificity. Unlike mechanisms such as the 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 others.
Memory. Again, unlike general defence mechanisms, an immune response against a particular antigen will usually generate immunological memory of that antigen. This means that the immune response on subsequent expo sures to the same antigen is generally faster and more powerful.
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Tolerance. The cells of the immune system are aggressive and potentially extretnely destructive. Control of their activity is essential for protection of healthy body tissues. As immune cells travel around the body, they check the marker proteins that cells show on their cell membranes. Healthy body cells display the expected self markers and are ignored by the patrolling immune cells However, non-self cells, such as cancer cells, foreign (transplanted) 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 make up 20-30% of circulating white blood cells but at any one time most of them are found in lym phatic and other tissues rather than in the bloodstream. They include natural killer cells involved in immunological surveillance, T-cells (the majority) and B-cells. T- and B-cells are responsible for immunity (specific defence) 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 antigens 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 (antigen specificity).
The hormone thymosin, produced by the thymus gland, is responsible for promoting T-cell maturation, which leads to the formation of fully specialised (differentiated), 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.
T-cells provide cell-mediated immunity, discussed below.
These are both produced and matured in the bone marrow. They produce antibodies (immunoglobulins), 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.
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 the body, it needs to be ‘presented’ to the T-cell on the surface of an antigen- presenting cell. There are different types of antigen- presenting cell, including macrophages. Macrophages are part of the non-specific 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 (present) 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 (non-self) 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 (clonal expansion). Four main types of specialized T-cell are produced, each of which is still directed against the original antigen, but which will tackle it in dil ent ways.
These directly inactivate any cells carrying antigens. Th attach themselves to the target cell and release power toxins, which are very effective because the two cells so close together. The main role of cytotoxic T-cells is destruction of abnormal body cells, e.g. infected cells and cancer 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). When helper T-cell numbers fall signifi- cantly, the whole immune system is compromised. T-helpers are the 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.
These cells act as ‘brakes’, turning off activated T- and B-cells. This limits the powerful and potentially damaging effects of the immune response. Suppressor T-cells are also thought to help prevent the development of auto-immunity and to protect the fetus in pregnancy.
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 enlarges and begins to divide (clonal expansion. It produces two functionally distinct types of cell, plasma cells and memory B-cells.
These secrete massive quantities of antibodies (immu- noglobulins, Ig) into the 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 origi- nally bound to the B-cell. Antibodies:
- bind to antigens, labelling them as targets for other defence cells such as cytotoxic T-cells and macrophages
- bind to bacterial toxins, neutralising them
- activate complement .
Like memory T-cells, these cells remain in the body long after the initial episode has been dealt with, and rapidly respond to another encounter with the same antigen by stimulating the production 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 exists between the immune reaction and its suppression. Autoimmune diseases are due to the disturbance of this balance.
The immune response to an antigen following the first exposure (primary immunisation) 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 acti- vate the T-cell system, which then stimulates B-cell divi- sion. Antibody levels 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 infection.
The secondary response. On 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.