Human body's immune response.

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Josephine G Paterson

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Abstract This article, which forms part of the life sciences series, explores the function of the immune system. It is important that nurses understand how the immune system works and its role in the prevention of infection. Innate and adaptive immunity are described and the differences between these two types of immune response are discussed. The acquisition and development of a competent immune system are also explored.

Authors Charles Hendry Retired, was senior lecturer, School of Nursing and Midwifery, University of Dundee. Alistair Farley Lecturer in nursing, School of Nursing and Midwifery, University of Dundee. Ella McLafferty Retired, was senior lecturer, School of Nursing and Midwifery, University of Dundee. Carolyn Johnstone Lecturer in nursing, School of Nursing and Midwifery, University of Dundee. Correspondence to: [email protected]

Keywords Adaptive immunity, allergy, autoimmune disorders, immune system, infection, innate immunity

Review All articles are subject to external double-blind peer review and checked for plagiarism using automated software.

Online Guidelines on writing for publication are available at www.nursing-standard.co.uk. For related articles visit the archive and search using the keywords above.

Function of the immune system Hendry C et al (2013) Function of the immune system. Nursing Standard. 27, 19, 35-42. Date of submission: July 12 2010; date of acceptance: March 3 2011.

There are many threats to the human body, including trauma, infection and exposure to toxic waste. Despite being exposed constantly to a large number of disease-causing microorganisms (pathogens) such as bacteria, fungi and viruses, most people remain free of infection for the majority of the time (murphy et al 2008). There are also threats from within the body in the form of abnormal cells. If not detected and destroyed, these cells may go on to develop into tumours and potentially pose a threat to health. This article examines the components of the immune system and how they function to provide protection against potentially harmful agents in the environment.

The immune system Tortora and Derrickson (2010) stated that ‘immunity or resistance is the ability to use our body’s defences to ward off damage or disease’. The immune system has several distinct but interrelated functions. These include to monitor, recognise, respond to and cease immune activity (Playfair and Bancroft 2004). The immune system monitors the body’s internal environment for the presence of any pathogens or changes in cells that may result in tumour formation. It is necessary that the immune system can distinguish self from non-self – the difference between the body’s cells and foreign matter or cells that have altered structurally. This is a key element of a healthy immune system. The body must not mount an immune response to healthy, intact body cells. however, it must recognise and respond to the presence of foreign matter or altered body cells (Playfair and Bancroft 2004, Janeway et al 2005).

although it works as an integrated whole, the immune system is composed of two distinct responses. These are:

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Haematopoietic stem cell

Myeloid cells

Granulocytes

��Neutrophils. ��Basophils. ��Eosinophils.

��Mast cells. ��Macrophages. ��Dendritic cells.

��Helper cells. ��Suppressor cells. ��Cytotoxic cells. ��Memory cells.

��Plasma cells. ��Memory cells.

Monocytes T cells B cells Natural killer cells

Lymphoid cells

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��Innate or non-specific immunity ��adaptive or specific immunity.

Figure 1 shows the origin of cells in the immune system.

Innate or non-specific immunity The innate immune system comprises cells and mechanisms, present from birth, which defend the host from infection by other organisms. The innate immune system provides an immediate, but non-specific response. Therefore, regardless of the level of threat from, for example, a harmful bacterium, innate immune responses are essentially the same in all circumstances (Seeley et al 2007). The innate immune response does not improve each time the body encounters a foreign substance. nonetheless, it is an effective first line form of defence.

Innate immune responses are many and varied, and include physical, mechanical and chemical barriers, such as intact skin and mucous membranes, lysosomal enzymes and gastric acid. actions such as crying, coughing, sneezing, intermittent bladder emptying and the movement of cilia in the respiratory tract also have a protective role. antimicrobial substances found in body fluids inhibit the growth of microorganisms. The action of phagocytes, such as neutrophils and macrophages, as well as large, granular lymphocytes called natural killer cells, also provide non-specific immunity. acute inflammation is the response of healthy tissue

to injury or infection and is a component of the innate immune response (Keogan et al 2006).

Physical, mechanical and chemical barriers The major physical, mechanical and chemical barriers to infection are the skin and mucous membranes that line the gastrointestinal, respiratory and genito-urinary tracts. according to Parham (2009): ��Intact skin is the major physical barrier to invading harmful organisms. In addition, the low ph of the skin, resulting from sweat and secretions from sebaceous glands, inhibits bacterial growth. ��The mucous membranes of the respiratory tract secrete a protective layer of mucus, which can trap harmful material. The movement of cilia in the respiratory tract, aided by coughing and sneezing reflexes, also helps prevent entry of pathogenic organisms. ��acid produced in the stomach limits the entry of harmful organisms, as does the antibacterial enzyme lysozyme, present in breast milk, tears, nasal secretions and saliva (Seeley et al 2008). The continual flow of tears and saliva also washes away debris that may encourage bacterial growth. ��Intermittent urinary bladder emptying flushes away organisms and the one-way flow of urine reduces the risk of microbes entering the bladder.

normal, commensal bacteria that inhabit the skin and the gastrointestinal and genito-urinary tracts prevent infection by pathogenic bacteria

FIGURE 1 Origin of cells in the immune system

(Adapted from Parham 2009)

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by competing with these infectious microorganisms for nutrients or attachment to suitable cell surfaces (Janeway et al 2005, murphy et al 2008). an organism that cannot establish itself on or in the human body cannot cause disease (Parham 2009).

Antimicrobial substances antimicrobial substances act by inhibiting microbial growth. There are four main types of antimicrobial substances: ��Interferons – these are a group of proteins produced by lymphocytes and macrophages when they are invaded by viruses. Interferons are involved in the activation of natural killer cells and macrophages (Seeley et al 2008). They also inhibit viral replication. ��Complement – this is a system involving a group of proteins found in the blood, which when activated forms the complement cascade. The complement cascade is a biochemical process in which one component activates the next component in the pathway. activated complement proteins provide protection from pathogens by promoting inflammation, chemotaxis and phagocytosis. The end product of the cascade is a protein-membrane attack complex that destroys the cell membranes of invading microorganisms (nairn and helbert 2007). ��Iron-binding proteins – these inhibit microbial growth by reducing the amount of iron available to certain bacteria. examples of iron-binding proteins include transferrin, ferritin and haemoglobin. Lactoferrin, found in milk, saliva and mucus, also reduces the amount of iron available to certain bacteria (Tortora and Derrickson 2010). ��antimicrobial proteins – these include dermcidin (produced by sweat glands) and defensins (produced by macrophages). They can destroy a wide range of microorganisms and attract other immune system cells such as mast cells, which release chemical mediators such as histamine that contribute to the inflammatory response (harder et al 2007).

Phagocytosis The process whereby certain cells engulf and destroy foreign cells or particles (microbial products) is known as phagocytosis (Figure 2). The two types of cell mostly responsible for phagocytosis are neutrophils and macrophages. eosinophils are capable of phagocytosis, but that is not their main function.

To adhere to and digest foreign material, the phagocyte must first be capable of recognising that the material is foreign. This can either happen

when the phagocyte binds to a carbohydrate residue present on the surface of a microorganism, or an antibody (immunoglobulin G (IgG)), which has already bound to the foreign microorganism. The binding of antibody to antigen marks it as a pathogen for destruction by phagocytosis and complement (Janeway et al 2005).

Once a phagocyte has recognised and made contact with a foreign microorganism invagination occurs, whereby the cell membrane forms a vesicle known as a phagosome. The phagocyte then engulfs the organism. The membrane surrounding the bacteria merges with the membrane of lysosomes in the phagocyte cytoplasm. Lysosomes contain degradative enzymes that destroy the pathogen and release digested microbial products (Playfair and Bancroft 2004).

Natural killer cells Between 5-15% of lymphocytes are natural killer cells, which can recognise tumour cells and body cells infected by a virus. They kill cells by releasing proteins that destroy the cell membrane (Keogan et al 2006).

Acute inflammatory response Inflammation occurs in response to any infection or injury. Signs of inflammation include redness,

FIGURE 2 Phagocytosis

jo A

N N

A C

A M

E R

o N

Macrophage

Debris

Release of digested microbial products

Engulfment

Phagosome

Bacteria

Macrophage

Digestion of phagocytosed microbial products

Invagination

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heat, swelling, pain and/or discomfort and impaired function of the affected area. When damaged, tissues respond by releasing histamine and other substances from injured cells, mast cells and basophils, promoting vasodilation (resulting in heat and redness) and increasing capillary permeability (increasing the amount of fluid entering the interstitial space), therefore causing oedema and pain. Inflammation is important because it increases the flow of blood to and from the site of infection or injury as well as enhancing the movement of leukocytes to the damaged area. accumulation and adhesion of leukocytes to the endothelium of blood vessel walls at the site of injury is known as margination.

The formation of fibrinogen clots around the site of injury effectively isolates the area from the surrounding healthy tissue, restricting damage and the spread of pathogenic organisms. In the early phase of inflammation, leucocytes migrate to the affected area as a result of chemotaxis. This migration is known as diapedesis. neutrophils begin to phagocytose bacteria and small pieces of damaged tissue. Subsequently, macrophages arrive at the site and are able to phagocytose greater quantities of bacteria and larger cells such as protozoa.

Lymphatic vessels are responsible for draining the injury site of excess fluid, cell debris and dead microorganisms. In addition, they bring antigens into contact with lymphocytes in the lymph nodes,

therefore initiating a specific immune response involving the recognition of antigens and the production of antibodies (murphy et al 2008). Figure 3 shows the acute inflammatory response.

Adaptive or specific immunity While providing a first line of defence, the innate immune response is non-specific. It would be wasteful for the body to be in a perpetual state of readiness to deal with any and all potentially harmful agents regardless of the likelihood of exposure. adaptive immunity involves a pathogen and antigen-specific response as and when required (Parham 2009).

The adaptive immune response involves leukocytes, classified as small lymphocytes. There are two types of small lymphocytes: B lymphocytes (B cells) and T lymphocytes (T cells). B cells and T cells originate from precursor haematopoietic stem cells in fetal bone marrow. Subsequently, some migrate via the blood to the thymus gland, where they undergo further development to become inactive T cells. B cells remain in the blood in an inactive form. The tissues of the thymus gland and bone marrow are called central or primary lymphoid tissues. The inactive B and T cells migrate via the blood to the peripheral lymphoid tissues (lymph nodes and spleen) and other lymphoid tissues. It is in these tissues that the lymphocytes meet antigens and become activated.

FIGURE 3 Acute inflammatory response

jo A

N N

A C

A M

E R

o N

Tissue injury

Microbes

Phagocytes

Diapedesis

Chemotaxis

Margination

Vasodilation

Increased permeability

Histamine, kinins, prostaglandins, leukotrienes and complement together stimulate vasodilation, increased permeability of blood vessels, chemotaxis, diapedesis and phagocytosis

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an antigen is any substance capable of provoking an immune response and is usually foreign to the organism (Playfair and Chain 2009).

It should be noted that lymphocytes spend only a few minutes in the blood during each circuit, compared with several hours in the lymphatic system, hence the critical role of the lymphatic system in preventing infection. Lymphocytes can also be found migrating to the tissues of the body. naive B cells (those that have still to encounter their relative antigen) live only a few days, whereas memory B cells (cells that remain in the body long after the initial immune response) and all T cells can live for months or years (Playfair and Bancroft 2004).

B cells after contact with an antigen, B cells mature into antibody secreting cells. The antigen receptors that are present on the surface of B cells are known as surface immunoglobulins (sIg). each cell has about 105 sIg molecules in its surface membrane. B cells bind to the antigen via their sIg molecules, which interact with complementary sites on the antigen (Delves et al 2006).

This binding of antigen and sIg results in a proliferation of the original B cells – the original B cell reproduces again and again until there are many thousands of cells all identical to the parent B cell. This is known as clonal expansion. The cloned B cells then undergo differentiation resulting in two different types of cell: memory cells and plasma cells. Plasma cells are found in the lymph nodes and only the antibodies they secrete pass out of lymph tissues and are transported in lymph and blood to the infected area. Plasma cells are responsible for secreting large amounts of immunoglobulin molecules that are chemically similar to the sIgs of the original B cell (Tortora and Derrickson 2010). The rate of secretion is about 2,000 antibody molecules per second for each plasma cell (Thibodeau and Patton 2010). These secreted immunoglobulins are the antibodies that can be detected in the blood. memory cells continue to circulate in the body long after the original exposure to the antigen (nairn and helbert 2007).

B cells present at birth are capable of reacting to any specific antigen, even before they come into contact with that antigen. This is because each B cell has a unique area of activated deoxyribonucleic acid, leading to the production of specific antibodies. During development, any B cells that have antibodies present on their surface corresponding to body cells are destroyed. This ensures that lymphocytes are tolerant of self – the immune system learns to recognise its own body cells and in effect ignores them (Playfair and Bancroft 2004).

antibodies are highly specific proteins produced by B cells in response to the presence of an antigen. The main function of antibodies is to bind to the antigen. antibodies belong to a group of plasma proteins known as gamma globulins. Because they form part of the immune system they are also called immunoglobulins. There are five different classes of antibodies produced in the body: IgG, Igm, Iga, IgD, and Ige (Table 1).

an antibody molecule is usually y-shaped and symmetrical, consisting of four polypeptide chains (Playfair and Chain 2009). each antibody molecule has a constant region, a hinge and a variable region. The variable regions have variable amino acid sequences – the part of the antibody that is unique and corresponds to a specific antigen. When the antibody meets the antigen they fit together like a key and a lock. as an antibody is y-shaped, it contains two binding sites – one on each arm of the y. This allows the antibody to combine with two antigen molecules and form antigen-antibody complexes (Keogan et al 2006).

antibodies combine with only one part of the antigen, known as an antigenic determinant site. most antigens have several antigenic determinant sites that are different from one another. This means that several different antibodies (originating from different B cell clones) can combine with the same antigen. most antigens are foreign substances and are not usually part of the chemistry of the body (Playfair and Chain 2009).

Action of secreted antibodies When secreted antibodies bind to their specific antigen they assist its destruction in several ways.

TABLE 1 Class and function of antibodies

Class Function

IgG Found in the blood and other body fluids. It enhances phagocytosis, neutralises toxins and protects against bacteria and viruses. It also crosses the placenta to protect the fetus.

IgM Found in blood and lymph. It is the first antibody to be produced during antigen and/or antibody response. It is effective against microbes and activates the complement system.

IgA Found mainly in the mucous membranes of the nose and throat, where it helps fight against respiratory allergens. It provides localised protection on mucosal surfaces. It is the main immunoglobulin found in tears, saliva, secretions from the gastrointestinal and genito-urinary tracts, and breast milk.

IgD Found in blood and lymph. It is involved in activation of B cells.

IgE Found in blood and located on mast cells and basophils. It is involved in the allergic response.

(Adapted from Roitt and Delves 2001)

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They exert most of their effects by enhancing the mechanisms of innate immunity. antibodies have two binding sites for an antigen, so a single antibody can bind together two antigens. many antibodies can cause large numbers of antigens to clump together, rendering them easier for macrophages and neutrophils to ingest. Bound antibodies can act as chemical markers or opsonins (antibodies that render bacteria and other cells susceptible to phagocytosis) on the surface of the antigen, therefore indicating that it should be targeted for destruction by phagocytosis. When bound to antigens, antibodies trigger the complement cascade, resulting in the production of the protein-membrane attack complex and cell lysis (Delves et al 2006). an important point to remember is that antibodies only initiate this response once they have bound to the antigen (Seeley et al 2008). Were this not so, free antibodies could trigger unnecessary immune reactions.

antibody-mediated immune responses are most effective against free-living pathogens, parasites and antigenic macromolecules in the circulation. These responses do not easily reach the many types of pathogens that live and replicate inside the cells of their host. T cells are the main defence against these pathogens (Playfair and Chain 2009).

T cells an antibody-like substance, which attaches itself to the surface of the T cell and acts as a receptor to a specific antigen, is also produced by T cells. as with B cells, T cells undergo a process of clonal expansion and differentiation when exposed to the appropriate stimulus. activation occurs when macrophages phagocytose an antigen and present it to the T cell. Sensitised T cells increase in size and divide, each giving rise to a clone (Playfair and Bancroft 2004).

The main functions of T cells are to: ��Kill body cells that have become infected with pathogens and are therefore inaccessible to antibodies. ��maintain an inflammatory response at the site of a persistent infection. ��regulate many features of acquired and innate immune responses.

These functions are achieved by four types of T cells: cytotoxic T cells, helper T cells, suppressor T cells and memory T cells.

Cytotoxic T cells are killer cells. They use toxic and perforin chemicals to kill the body’s cells when they become infected with intracellular pathogens (Parham 2009). They will not function unless bound to an antigen and stimulated by helper T cells (Playfair and Bancroft 2004).

helper T cells exert a regulatory influence. They are able to activate the adaptive immune response, increasing its rate and intensity, and boosting the effectiveness of the innate immune response (Playfair and Bancroft 2004). In particular, they prolong the inflammatory reaction. helper T cells also regulate the overall immune response by activating suppresser T cells when the immune reaction is no longer required. helper T cells achieve this wide range of effects by secreting a series of chemicals known as lymphokines. Lymphokines are, in effect, hormones that regulate the immune response (Delves et al 2006). There are about 20 of these hormones in total.

helper T cells are activated after contact with an antigen and following a signal from macrophages. This is an example of the integration of the innate and acquired immune responses. after stimulation by helper T cells, suppresser T cells dampen the immune response by reducing the activity of B cells and other T cells. They do this by secreting their own lymphokines, which are sometimes referred to as suppresser factors (Playfair and Bancroft 2004).

Primary and secondary immune responses When antigens are encountered for the first time, a primary immune response occurs. This is the initial response mounted by the immune system on first encountering a foreign antigen. however, the immune system generally responds more rapidly and effectively when an antigen is presented on subsequent occasions. This is known as the secondary immune response and is characterised by a rapid memory B cell response. every subsequent encounter with a familiar antigen results in rapid activation of memory B and/or T cells, which produce large numbers of plasma cells, and/or helper and cytotoxic T cells (Delves et al 2006).

There are two different aspects of adaptive immunity, namely cell-mediated and humoral immunity. Cell-mediated immunity, which refers to immune responses directed at infected body cells, is mediated by T cells. humoral immunity refers to immune responses directed at pathogens in body fluids, and is mediated by B cells and their secreted antibodies (Keogan et al 2006).

There are three main differences between the primary and secondary immune responses, which are (Delves et al 2006, Seeley et al 2008, Parham 2009): ��During the primary immune response there is a lag of about three to 14 days before detectable levels of antibody appear in the serum,

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compared to a lag of only a few hours to three days in the secondary immune response. ��antibody concentration rises more rapidly and reaches higher levels during the secondary immune response. ��antibody levels decline more slowly after a secondary immune response, sometimes persisting for months and even years.

Immune acquisition a limited degree of immunity is present at birth, but most immunity is acquired over the first few years of life (Parham 2009). Vaccination programmes and exposure to pathogens in later life enhance overall immunity. Immunity can be acquired actively and passively. This can be further classified by whether immunity is acquired naturally or artificially (Box 1). Immunisation stimulates an immune response by subjecting the individual to a modified version of the pathogen that causes disease. This immune response is achieved by injecting the desired antigen after it has been suitably modified to render it harmless. It may be necessary to have a course of injections before the immune response is complete or to receive a booster injection periodically to maintain sufficiently high levels of an antibody (Thibodeau and Patton 2010).

Changing immune competence humans are not born with full immune competence. although the cells responsible for all types of immune response are detectable in the fetus, they must continue to mature for up to two years until a level of immunity comparable to the adult is reached.

The immune system is as prone as other systems of the body to degenerative change. as a consequence, older adults become more susceptible to new infections and the immune response is not as vigorous, nor as swift. It has also been suggested that the immune system has a role in the detection and eradication of cells that begin to grow abnormally and which, if left unchecked, might become cancerous. For this to occur, abnormal cells would have to be antigenic and, to date, tumour cells appear to be only weakly antigenic in that they stimulate a weak immune response (Keogan et al 2006).

Immune system failure Failure of the immune system can result in a range of disorders.

Hypersensitivity or allergy The conditions hypersensitivity or allergy occur when a person’s immune system reacts to substances that are harmless to most individuals (hendry and Farley 2001, Tortora and Derrickson 2010). One in three people is likely to develop an allergy at some time in their lives (Delves et al 2006). Some people develop a severe, potentially life-threatening allergy to some antigens, for example peanuts. This extreme allergic reaction is known as anaphylaxis or anaphylactic shock.

Autoimmune disorders When the immune system fails to distinguish self from non-self, autoimmune disorders occur (Farley and hendry 2002) (Box 2). If the immune system is no longer able to recognise cells that are part of an individual’s normal make up, the immune system may target the body’s own cells, tissues and organs, causing damage and affecting function.

BOX 1 Types of acquired immunity

Passive (natural): ��Via the placenta – maternal antibodies (IgG) provide short-term protection of about six months against ailments that the mother experienced during her life, for example chickenpox and measles (Parham 2009). ��Via breast milk – antibodies in the mother’s milk (IgA) provide short-term protection of about six months against gastrointestinal infections (Parham 2009).

Passive (artificial): ��Immune serum – serum of a previously infected person is taken and treated to yield antibodies to the infection in question, which are then administered to the individual exposed to infection. Immunity gained in this way is immediate, but lasts only a few weeks. Immune serum is useful against, for example, botulism, rabies and venom from snakes and spiders (Seeley et al 2007).

Active (natural): ��Clinical or sub-clinical infective episodes, in other words a primary or secondary immune response.

Active (artificial): ��Immunisation – stimulating an immune response by exposing the individual to weakened or dead strains of the organism that the person requires protection from. A course of injections is often required.

BOX 2 Autoimmune disorders

��Systemic diseases, for example systemic lupus erythematosus. ��Rheumatoid arthritis. ��organ specific disorders, such as Hashimoto’s thyroiditis. ��Diabetes mellitus (type 1). ��Multiple sclerosis.

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This could result in disease of specific tissues and organs, or it might have a systemic effect. an example of a systemic disease is systemic lupus erythematosus – a chronic inflammatory disease affecting a range of different body systems.

Individuals do not generally produce potentially harmful antibodies that are a match for antigens

References Delves Pj, Martin Sj, Burton DR, Roitt IM (2006) Roitt’s Essential Immunology. Eleventh edition. Blackwell Publishing, Massachusetts MA.

Farley A, Hendry C (2002) Autoimmune disorders. Nursing Standard. 16, 41, 38-40.

Harder j, Glaser R, Schroder j (2007) Review: human antimicrobial proteins – effectors of innate immunity. Journal of Endotoxin Research. 13, 6, 317-338.

Hendry C, Farley AH (2001) Understanding allergies and their treatment. Nursing Standard. 15, 35, 47-52.

janeway CA, Travers P, Walport M, Shlomchik Mj (2005) Immunobiology. The Immune System in Health and Disease. Sixth edition. Churchill Livingstone, New York NY.

Keogan MT, Wallace EM, o’Leary P (2006) Concise Clinical Immunology for Healthcare Professionals. Routledge, Abingdon.

Murphy K, Travers P, Walport M (2008) Janeway’s Immunology. Seventh edition. Garland Science, New York NY.

Nairn R, Helbert M (2007) Immunology for Medical Students.

Second edition. Mosby Elsevier, Philadephia PA.

Parham P (2009) The Immune System. Third edition. Garland Science, London.

Playfair jHL, Bancroft Gj (2004) Infection and Immunity. Second edition. oxford University Press, oxford.

Playfair jHL, Chain BM (2009) Immunology at A Glance. Ninth edition. Wiley Blackwell, Chichester.

Roitt IM, Delves Pj (2001) Roitt’s Essential Immunology. Tenth edition. Blackwell Science, oxford.

Seeley RR, Stephens TD, Tate P (2007) Essentials of Anatomy and Physiology. Sixth edition. McGraw Hill, Boston MA.

Seeley RR, Stephens TD, Tate P (2008) Anatomy and Physiology. Eighth edition. McGraw Hill, Boston MA.

Thibodeau GA, Patton KT (2010) Anatomy and Physiology. Seventh edition. Mosby Elsevier, St Louis, Mo.

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GLOSSARY Antibody A highly specific protein secreted by B lymphocytes following exposure to an antigen. Antigens Substances that can stimulate an immune response. Chemotaxis A process by which the release of chemicals attracts defence cells, for example leukocytes, to the site of infection or injury. Immunoglobulin A protein specifically associated with the immune system. Protozoa Single-celled organisms larger than bacteria, which often infect human tissues.

POINTS FOR PRACTICE ��Identify and locate local guidelines on response to anaphylaxis and familiarise yourself with them. Locate any emergency equipment that you may need in the event that a patient presents with anaphylaxis. ��It is the nurse’s responsibility to minimise infection risks in the external environment. Consider the main risk factors in your workplace and identify what action you could take to minimise them. ��As stated within the article, normal, commensal bacteria that inhabit the skin and the gastrointestinal and genito-urinary tracts compete with and prevent infection by pathogenic bacteria. outline how a patient who has had antibiotic therapy might subsequently develop Clostridium difficile.

present in their own body cells. In this way, the body’s defence system learns to distinguish self from non-self and automatically ignores its own tissues. The ability to differentiate self from non-self is called tolerance. The development of tolerance occurs during fetal development and is the result of clonal deletion or inactivation of developing lymphocytes. a clone is a genetically identical group of B or T cells that respond to a specific trigger. at birth, the immune system no longer has any small lymphocytes that will respond to its own body cells – it has learned to distinguish self from non-self. Inability to tolerate one’s body cells can affect specific organs in the body or lead to a systemic disorder (Tortora and Derrickson 2010).

Conclusion Despite being exposed to a large number of disease-causing microorganism, such as bacteria, fungi and viruses, most people remain free of infection for the majority of the time. This is the result of a healthy and effective immune system. In this article, the components of the immune system and how they function to provide protection against potentially harmful agents in the environment have been examined. The differences between innate and adaptive immunity and the way in which they work together have been discussed. By understanding the way in which the immune system works, nurses are better able to appreciate the need for infection control polices and guidance, and to support patients in mounting an effective response to harmful microorganisms NS

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