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Learning Resources - Immune System - Revision Notes


  • Non-specific Defence Mechanisms

    • Protect against any possible dangers


  • Specific Defence Mechanisms

    • Grouped together under the term immunity
      • Resistance is directed against only one specific invader
        • Immunological memory develops – confers long-term immunity to specific infections
          • An antigen is anything that stimulates an immune response


      • Non-specific Defence Mechanisms

      • First lines of general defence - Prevent entry and minimise further passage of microbes and other foreign material into the body
    • Five main non-specific defence mechanisms
      • Defence at body surfaces
        • Phagocytosis
        • Natural antimicrobial response
          • Immunological surveillance


          Defence at Body Surfaces

          When skin and mucous membrane are intact and healthy they provide an efficient physical barrier to invading microbes


          Outer layer of skin can be penetrated by only a few types of microbe


          The mucus secreted by the 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 the cilia in the respiratory tract moves the mucus and inhaled foreign material towards the throat


          Then coughed up or swallowed


          The one-way flow of urine from the bladder minimise's the risk of microbes ascending through the urethra into the bladder



          Process of phagocytosis = cell eating

          Phagocytic defence cells (macrophages and neutrophils) migrate to sites of inflammation and infection (chemotaxis)

          Because neutrophils and invading microbes release chemicals that attract them (chemoattractants)

          Phagocytes trap particles either by engulfing them with their body mass or by extending long pseudopodia towards them – these grasp them the reel them in

          These cells are non-selective in their targets

          They will bind, engulf and digest foreign cells or particles

          Macrophages have an important role as a link between non-specific and specific defence mechanisms

          After ingestion and digestion of an antigen they act as antigen-presenting cells, displaying their antigen on their own cell surface to stimulate T-lymphocytes and activate the immune response


          Natural Antimicrobial Substances

          Hydrochloric acid

          Present in high concentrations in the gastric juice


          Small protein with antibacterial properties

          Present in




          Present in nasal secretions and saliva

          Inactivate microbes


          Secreted into the mouth and washes away food debris that may otherwise encourage bacterial growth


          Substances produces by T-lymphocytes and by cells that have been invaded by viruses

          Prevent viral replication within infected cells and also the spread of viruses to healthy cells


          System of about 20 proteins found in the blood and tissues

          Activated by the presence of immune complexes - An antigen and antibody bound together

          Also activated by foreign sugars on bacterial cell walls

          Binds to and damages bacterial cell walls – destroying the microbe

          Binds to bacterial cells walls – stimulating phagocytosis by neutrophils and macrophages

          Attracts phagocytic cells such as neutrophils into an area of infection – stimulates chemotaxis


          The Inflammatory Response

          Physiological response to tissue damage and is accompanied by a characteristic series of local changes

          Most commonly takes place when microbes have overcome other non-specific defence mechanisms

          Purpose is protective

          To isolate, inactivate and remove both the causative agent and damaged tissue so that healing can occur

          Inflammatory conditions are recognised by their Latin name ‘itis’




          Causes of Inflammation







          Physical agents



          Mechanical injury

          Ultraviolet and ionising radiation


          Chemical agents


          Microbial toxins

          Organic poisons – weedkillers





          Acute Inflammation

          Usually short-term

          Range from mild to very severe

          Signs of inflammation





          Loss of function

          Most aspects of the inflammatory response are beneficial – promoting removal of harmful agents and setting the scene for healing

          Acute inflammatory response is a collection of overlapping events

          Increased blood flow

          Accumulation of tissue fluid

          Migration of leukocytes

          Increased core temperature




          Increased Blood Flow

          Following injury both the arterioles supplying the damaged area and the local capillaries dilate – increasing blood flow to the site

          Caused mainly by the local release of a number of chemical mediators from damaged cells



          Increased blood flow provides more oxygen and nutrients for the increased cellular activity that accompanies inflammation


          Increased temperature

          Reddening of an inflamed area

          Contributes to the swelling and oedema associated with inflammation


          Increased Tissue Fluid Formation

          Swelling (oedema) of the damaged tissues is caused by fluid leaving local blood vessels and entering the interstitial spaces

          Partly due to increased capillary permeability caused by




          Also due to elevated pressure inside the vessels – because of increased flow


          Most excess fluid drains away in the lymphatic vessels – they also drain away

          Damaged tissue

          Dead and dying cells



          Plasma proteins also escape into the tissues through the leaky capillary walls – increases osmotic pressure of the tissue fluid and draws more fluid out of the blood

          Proteins include:


          Fibrinogen – clotting protein

          Fibrinogen in the tissues is converted by thromboplastin to fibrin – forms an insoluble mesh within the interstitial space walling off the inflamed area – helps to limit the spread of any infection


          Migration of Leukocytes

          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 pre-dominant 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 the neutrophils

          They phagocytose dead/dying tissue, microbes and other antigenic material and also dead/dying neutrophils


          Some microbes resist digestion and provide a possible source of future infection


          Increased Core Temperature

          Inflammatory response may be accompanied by a rise in body temperature (pyrexia) especially if these is significant infection


          Body temperature rises when an endogenous pyrogen is released from macrophages and granulocytes in response to microbial toxins or immune complexes


          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 twin benefits

          Inhibits growth and division of microbes

          Promotes the activity of phagocytes



          This occurs when local swelling compresses sensory nerve endings


          Exacerbated by chemical mediators of the inflammatory process



          These potentiate the sensitivity of the sensory nerve endings to painful stimuli


          Although pain is unpleasant – may indirectly promote healing

          It encourages protection of the damaged site


          Suppuration (Pus Formation)

          Pus consists of:

          Dead phagocytes

          Dead cells

          Cell debris


          Inflammatory exudate

          Living and dead microbes


          Contained within a membrane of new blood capillaries, phagocytes and fibroblasts


          Most common causative pyogenic (pus-forming) microbes are

          Staphylococcus aureus

          Streptococcus pyogenes


          Small amounts of pus from boils and large amounts from abscesses S.aureus produces the enzyme coagulase

          Converts fibrinogen to fibrin – localises the pus


          S.pyogenes produces toxins that break down tissue, causing spreading infection


          Healing, following pus formation is by secondary intention


          Superficial abscesses tend to rupture and discharge pus through the skin – healing is usually complete unless tissue damage is extensive


          Deep-seated abscesses may have a variety of outcomes

          Early rupture with complete discharge of pus on to the surface – followed by healing


          Rupture and limited discharge of pus on to the surface – followed by the development of a chronic abscess with an infected open channel or sinus


          Rupture and discharge of pus into an adjacent organ or cavity, forming an infected channel open at both ends or fistula


          Eventual removal of pus by phagocytes – followed by healing


          Enclosure of pus by fibrous tissue that may become calcified, harbouring live organisms which may become a source of future infection


          Formation of fibrous adhesions between adjacent membranes



          Shrinkage of fibrous tissue as it ages, which may reduce the lumen or obstruct a tube



          Blood vessel


          Chronic Inflammation

          More tissue is likely to be destroyed


          Inflammatory cells are mainly lymphocytes


          Fibroblasts are activated – leading to the laying down of collagen and fibrosis


          If the body defences are unable to clear the infection they may try to wall it off

          Forming nodules called granulomas - These contain collections of defensive cells


          Chronic inflammation may either be

          A complication of acute inflammation

          Following chronic exposure to an irritant


          Immunological Surveillance

          Population of lymphocytes (natural killer 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

          These are recognised by the natural killer cells

          They immediately kill the cell



          Cell type involved in immunity is the lymphocyte


          This white blood cell is manufactured in the bone marrow and had a large single nucleus


          Once released into the bloodstream from the bone marrow lymphocytes are further processed to make two functionally distinct types


          Processed by the thymus gland

          Hormone Thymosin is responsible for promoting the processing which leads to the formation of fully specialised, mature, functional T-lymphocytes

          Mature T-lymphocytes have been programmed to recognise only one type of antigen – the chickenpox virus

          T-lymphocytes provide cell-mediated immunity


          Produced and processed in the bone marrow

          Role is production of antibodies (immunoglobulins) – proteins designed to bind to and destroy an antigen

          Each B-lymphocyte targets one specific antigen – the antibody released reacts with one type of antigen and no other

          B-lymphocytes provide antibody-mediated immunity


          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

          the antigen has come from outside the body it needs to be ‘presented’ to the T-lymphocyte 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 – they also participate in immune responses

          After digesting the antigen they transport the most antigenic fragment to their own cell membrane and display it on their surface

          Within the circulation they eventually come into contact with the T-lymphocyte that has been processed to target that particular antigen

          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-lymphocyte


          Whichever way the antigen is presented to the T-lymphocyte, it stimulates the division and proliferation (clonal expansion) of the T-lymphocyte


          Four main types of specialised T-lymphocyte are produced each of which is still directed against the original antigen – tackles it in different ways

          Memory T-cells:

          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

          Cytotoxic T-cells:

          Directly inactivate any cells carrying antigens

          They attach themselves to the target cell and release powerful toxins – very effective because the two cells are so close together

          Main role is destruction of abnormal body cells

          Helper T-cells:

          Essential for correct functioning of cell-mediated immunity and also antibody-mediated immunity

          Main role in immunity is emphasised in situations where they are destroyed as by the human immunodeficiency virus (HIV)

          When helper T-lymphocyte numbers fall significantly they whole immune system is compromised

          T-helpers are the commonest of the T-lymphocytes

          Main functions include:

          Production of special chemicals called cytokines

          Cooperating with B-lymphocytes to produce antibodies

          Suppressor T-cells:

          Act as ‘brakes’ turning off activated T and B-lymphocytes

          Limits the powerful and potentially damaging effects of the immune response


          Antibody-mediated (Humoral) Immunity

          B-lymphocytes are fixed in lymphoid tissue


          Lymph nodes


          B-lymphocytes 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 a helper T-lymphocyte the B-lymphocyte enlarges and begins to divide


          Produces two functionally distinct types of cell

          Plasma cells:

          Secrete antibodies into the blood

          Antibodies are carried throughout the tissues, while B-lymphocytes themselves remain fixed in lymphoid tissue

          Live no longer than a day

          Produce only one type of antibody which targets the specific antigen that originally body to the B-lymphocyte


          Bind to antigen – labelling then as targets for other defence cells such as cytotoxic T-lymphocytes and macrophages

          Bind to bacterial toxins, neutralising them

          Activate complement

          Memory B-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

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