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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

           

          Phagocytosis

          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

          Lysozyme

          Small protein with antibacterial properties

          Present in

          Granulocytes

          Tears

          Antibodies

          Present in nasal secretions and saliva

          Inactivate microbes

          Saliva

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

          Interferons

          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

          Complement

          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’

          Appendicitis

          Laryngitis

           

          Causes of Inflammation

          Microbes

          Bacteria

          Viruses

          Protozoa

          Fungi

           

          Physical agents

          Heat

          Cold

          Mechanical injury

          Ultraviolet and ionising radiation

           

          Chemical agents

          Organic

          Microbial toxins

          Organic poisons – weedkillers

          Inorganic

          Acids

          Alkalis

           

          Acute Inflammation

          Usually short-term

          Range from mild to very severe

          Signs of inflammation

          Redness

          Heat

          Pain

          Swelling

          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

          Pain

          Suppuration

           

          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

          Histamine

          Serotonin

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

          Causes

          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

          Histamine

          Serotonin

          Prostaglandins

          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

          Toxins

           

          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:

          Antibodies

          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

           

          Pain

          This occurs when local swelling compresses sensory nerve endings

           

          Exacerbated by chemical mediators of the inflammatory process

          Bradykinin

          Prostaglandins

          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

          Fibrin

          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

          Pleura

          Peritoneum

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

          Oesophagus

          Bowel

          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

           

          Immunity

          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

          T-lymphocyte:

          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

          B-lymphocyte:

          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

          Spleen

          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

          Antibodies:

          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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