File Name: anatomy and physiology of immune system .zip
T cells also called T lymphocytes are one of the major components of the adaptive immune system. Their roles include directly killing infected host cells, activating other immune cells, producing cytokines and regulating the immune response. This article will discuss the production of T cells, the different types present in the immune system and relevant clinical conditions. T lymphocytes originate from haematopoietic stem cells which are produced in the bone marrow.
From the months spent in the womb to the end of his life, every individual is under constant attack from an enormous range of potentially harmful invaders. These threats include such diverse entities as bacteria, viruses, cancer cells, parasites and foreign non-self cells, e. The body has therefore developed a wide selection of protective measures, which can be divided into two categories.
These are grouped together under the term immunity. Resistance is directed against only one specific invader. These are the first lines of general defence; they prevent entry and minimise further passage of microbes and other foreign material into the body.
Few pathogens can establish themselves on healthy skin. Mucus secreted by mucous membranes traps microbes and other foreign material on its sticky surface.
Sebum and sweat secreted onto the skin surface contain antibacterial and antifungal substances. Hairs in the nose act as a coarse filter, and the sweeping action of cilia in the respiratory tract moves mucus and inhaled foreign materials towards the throat.
Then it is coughed up or swallowed. The one-way flow of urine from the bladder minimises the risk of infection ascending through the urethra into the bladder. Phagocytic defence cells such as macrophages and neutrophils migrate to sites of inflammation and infection chemotaxis , because neutrophils themselves and invading microbes release chemicals that attract them chemoattractants. Phagocytes trap particles either by engulfing them Fig.
These cells are non-selective in their targets; they bind, engulf and digest foreign cells or particles. Macrophages have an important role as a link between the non-specific and specific defence mechanisms. This is present in high concentrations in gastric juice, and kills the majority of ingested microbes. This is a small protein with antibacterial properties present in granulocytes, tears, and other body secretions, but not in sweat, urine or cerebrospinal fluid.
This is secreted into the mouth and washes away food debris that may otherwise encourage bacterial growth. Its slightly acid medium is antibacterial. These chemicals are produced by T-lymphocytes and by cells that have been invaded by viruses. They prevent viral replication within infected cells, and the spread of viruses to healthy cells. Complement is a system of about 20 proteins found in the blood and tissues.
It is activated by the presence of immune complexes an antigen and antibody bound together and by foreign sugars on bacterial cell walls. The inflammatory response. This is the physiological response to tissue damage and is accompanied by a characteristic series of local changes Fig.
It most commonly takes place when microbes have overcome other non-specific defence mechanisms. Its purpose is protective: to isolate, inactivate and remove both the causative agent and damaged tissue so that healing can take place.
The cardinal signs of inflammation are redness, heat, swelling and pain. Acute inflammation is typically of short duration, e. Most aspects of the inflammatory response are hugely beneficial, promoting removal of the harmful agent and setting the scene for healing to follow. The acute inflammatory response is described here as a collection of overlapping events: increased blood flow, accumulation of tissue fluid, migration of leukocytes, increased core temperature, pain and suppuration.
Following injury, both the arterioles supplying the damaged area and the local capillaries dilate, increasing blood flow to the site. This is caused mainly by the local release of a number of chemical mediators from damaged cells, e. Increased blood flow to the area of tissue damage provides more oxygen and nutrients for the increased cellular activity that accompanies inflammation.
Increased blood flow causes the increased temperature and reddening of an inflamed area, and contributes to the swelling oedema associated with inflammation. One of the cardinal signs of inflammation is swelling of the tissues involved, which is caused by fluid leaving local blood vessels and entering the interstitial spaces.
This is partly due to increased capillary permeability caused by inflammatory mediators such as histamine, serotonin and prostaglandins, and partly due to elevated pressure inside the vessels because of increased flow. Most of the excess tissue fluid drains away in the lymphatic vessels, and takes damaged tissue, dead and dying cells, and toxins with it.
Plasma proteins, normally retained within the bloodstream, also escape into the tissues through the leaky capillary walls; this increases the osmotic pressure of the tissue fluid and draws more fluid out of the blood. Some pathogens, e. Streptococcus pyogenes , which causes throat and skin infections, release toxins that break down this fibrin network and promote spread of infection into adjacent, healthy tissue.
Sometimes tissue oedema can be harmful. For instance, swelling around respiratory passages can obstruct breathing, and significant swelling often causes pain. On the other hand, the swelling around a joint cushions it and limits movement, which encourages healing. Loss of fluid from the blood thickens it, slowing flow and allowing the normally fast-flowing white blood cells to make contact with, and adhere to, the vessel wall.
Phagocyte activity is promoted by the raised temperatures local and systemic associated with inflammation.
After about 24 hours, macrophages become the predominant cell type at the inflamed site, and they persist in the tissues if the situation is not resolved, leading to chronic inflammation.
Macrophages are larger and longer lived than neutrophils. Some microbes resist digestion and provide a possible source of future infection, e. Mycobacterium tuberculosis. This is the chemical attraction of leukocytes, including neutrophils and macrophages, to an area of inflammation. It may be that chemoattractants act to retain passing leukocytes in the inflamed area, rather than actively attracting them from distant areas of the body.
Known chemoattractants include microbial toxins, chemicals released from leukocytes, prostaglandins from damaged cells and complement proteins.
The inflammatory response may be accompanied by a rise in body temperature pyrexia , especially if there is significant infection. Body temperature rises when an endogenous pyrogen interleukin 1 is released from macrophages and granulocytes in response to microbial toxins or immune complexes.
Interleukin 1 is a chemical mediator that resets the temperature thermostat in the hypothalamus at a higher level, causing pyrexia and other symptoms that may also accompany inflammation, e. Pyrexia increases the metabolic rate of cells in the inflamed area and, consequently, there is an increased need for oxygen and nutrients.
The increased temperature of inflamed tissues has the twin benefits of inhibiting the growth and division of microbes, whilst promoting the activity of phagocytes.
This occurs when local swelling compresses sensory nerve endings. It is exacerbated by chemical mediators of the inflammatory process, e. Although pain is an unpleasant experience, it may indirectly promote healing, because it encourages protection of the damaged site. Pus consists of dead phagocytes, dead cells, fibrin, inflammatory exudate and living and dead microbes. This occurs when the cause has been successfully overcome.
Damaged cells and residual fibrin are removed, being replaced with new healthy tissue, and repair is complete, with or without scar formation. Acute inflammation may become chronic if resolution is not complete, e. The processes involved are very similar to those of acute inflammation but, because the process is of longer duration, considerably more tissue is likely to be destroyed.
Tuberculosis is an example of an infection that frequently becomes chronic, leading to granuloma formation. Chronic inflammation may either be a complication of acute inflammation see above or follow chronic exposure to an irritant. A population of lymphocytes, called natural killer NK cells, constantly patrol the body searching for abnormal cells.
Cells that have been infected with a virus, or mutated cells that might become malignant, frequently display unusual markers on their cell membranes, which are recognised by NK cells. Having detected an abnormal cell, the NK cell immediately kills it. Although NK cells are lymphocytes, they are much less selective about their targets than the other two types discussed in this chapter T- and B-cells.
If these are overwhelmed, activation of the powerful immune system follows. Immunity possesses two key attributes not seen with non-specific defences: specificity and memory.
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. 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 exposures to the same antigen is generally faster and more powerful. The cell type involved in immunity is the lymphocyte p. This long-lived white blood cell is manufactured in the bone marrow, and has a characteristically large, single nucleus. Once released into the bloodstream from the bone marrow, lymphocytes are further processed to make two functionally distinct types: the T-lymphocyte and the B-lymphocyte.
For each of the millions of possible antigens that might be encountered in life, there is a corresponding T- and B-lymphocyte 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.
These are processed by the thymus gland p. The hormone thymosin, produced by the thymus, is responsible for promoting the processing, which leads to the formation of fully specialised differentiated , mature, functional T-lymphocytes.
It is important to recognise that a mature T-lymphocyte 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-lymphocyte manufactured to recognise the chickenpox virus will not react to a measles virus, a cancer cell, or a tuberculosis bacterium. These are both produced and processed in the bone marrow. They produce antibodies immunoglobulins , which are proteins designed to bind to, and destroy, an antigen. As with T-lymphocytes, each B-lymphocyte targets one specific antigen; the antibody released reacts with one type of antigen and no other. Cell-mediated immunity. T-lymphocytes that have been activated in the thymus gland are released into the circulation.
When they encounter their antigen for the first time, they become sensitised to it. There are different types of antigen-presenting cell, including macrophages. After digesting the antigen they transport the most antigenic fragment to their own cell membrane and display it on their surface Fig.
They display present this antigen to the T-lymphocyte that has been processed to target that particular antigen, which results in activation of 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-lymphocyte.
Whichever way the antigen is presented to the T-lymphocyte, it stimulates the division and proliferation clonal expansion of the T-lymphocyte Fig. Four main types of specialised T-lymphocyte are produced, each of which is still directed against the original antigen, but which will tackle it in different ways.
All organisms are connected in a complex web of relationships. Although many of these are benign, not all are, and everything alive devotes significant resources to identifying and neutralizing threats from other species. From bacteria through to primates, the presence of some kind of effective immune system has gone hand in hand with evolutionary success. This article focuses on mammalian immunity, the challenges that it faces, the mechanisms by which these are addressed, and the consequences that arise when it malfunctions. The problems that the mammalian immune system solves are not restricted to higher animals; they are faced by all forms of life and are ignored by none. The pressure that natural selection exerts is inexhaustible and unending. Emerging infectious diseases have as much potential to shape future human history as the epidemics and pandemics of the past.
The immune system includes primary lymphoid organs, secondary lymphatic tissues and various cells in the innate and adaptive immune systems. The key primary lymphoid organs of the immune system include the thymus and bone marrow, as well as secondary lymphatic tissues including spleen, tonsils, lymph vessels, lymph nodes, adenoids, skin, and liver. The thymus is largest and most active during the neonatal and pre-adolescent periods of development. By the early teens, the thymus begins to atrophy and thymic stroma is replaced by adipose tissue. Nevertheless, residual T-lymphopoiesis continues throughout adult life. Bone marrow is the flexible tissue found in the interior of bones. In humans, red blood cells are produced in the heads of long bones.
From the months spent in the womb to the end of his life, every individual is under constant attack from an enormous range of potentially harmful invaders. These threats include such diverse entities as bacteria, viruses, cancer cells, parasites and foreign non-self cells, e.
Ideally, the immune response will rid the body of a pathogen entirely. The adaptive immune response, with its rapid clonal expansion, is well suited to this purpose. Think of a primary infection as a race between the pathogen and the immune system. During the first 4 to 5 days, the innate immune response will partially control, but not stop, pathogen growth. As the adaptive immune response gears up, however, it will begin to clear the pathogen from the body, while at the same time becoming stronger and stronger.
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