AQA Biology AS Unit 1: Immunity

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6 Immunity

6.1 Defence Mechanisms

  • Immunity: the means by which the body protects itself against infection
  • The two main types of immunity are:
    • Non-specific: mechanisms that don't distinguish between pathogens but respond to all of them in the same way, they act immediately and take two forms:
      • Barrier to entry of pathogens
      • Phagocytosis
    • Specific mechanisms: distinguish between pathogens, response is less rapid but provides long lasting immunity. Involves white blood cells called lymphocyte and take two forms:
      • Cell mediated responses involving T lymphocytes
      • Humoral responses involving B lymphocytes
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Defence Mechanisms Continued

Recognising your own Cells

  • Without lymphocytes knowing your own cells and chemicals they would destroy them
  • Specific lymphocytes already exist they are not create due to infection
  • Due to the amount of these lymphocytes there is a high probability  that one of the lymphocytes will have a protein on its surface complementary to a pathogen
  • When infection occurs the lymphocyte complementary to the pathogen is stimulated to build up its numbers so it can destroy the pathogen
  • This explains the time lag between exposure to the pathogen and the body defences stopping it
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6.2 Phagocytosis

Barriers to Entry

  • Protective Covering: Skin covers body surface providing a physical barrier hard to penetrate for most pathogens
  • Epithelia covered in mucus: pathogens stick to mucus which is than transported to by cilia up to the trachae where it is swallowed into the stomach
  • Stomach acid: Enzymes of most pathogens are denatured in the stomach and then killed

Phagocytosis

  • Large particles e.g. bacteria are too big t cross cell surface membranes by diffusion or active transport
  • Instead have to be engulfed by cells in the form of vesicles formed from cell surface membrane: phagocytosis
  • In blood the white blood cells that carry out phagocytosis are phagocytes
  • They provide defence against pathogens
  • Some phagocytes travel in blood but can move out into other tissues
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Phagocytosis Continued

Summary of Phagocytosis

  • Chemicals of pathogen act as attractants causing phagocytes to move towards them
  • Phagocytes attach themselves to the pathogen surface
  • They engulf the pathogen to form a vesicle: phagosome
  • Lysosomes move towards the vesicle and fuse
  • Enzymes within the lysosomes break down pathogen similar to the hydrolysis of large insoluble molecules
  • Soluble products from breakdowm of pathogen are absobed into cytoplasm of the phagocyte
  • Phagocytosis causes inflammation at the site of infection, swollen area contains dead pathogens and phagocytes known as pus
  • Inflammation is caused my histamine which causes dilation of the blood vessels; this speeds up delivery of phagocytes to the site of infection
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6.3 T cells and cell-mediated Immunity

Antigens

  • Part of organism recognised as non-self (foreign) by immune system, it stimulates the immune response
  • Usually proteins part of cell surface membranes or cell walls of invading cells
  • Antigen triggers antibody production

Lymphocytes

  • Phagocytosis is non-specific
  • Specific reactions are slower and depend on lymphocytes
  • There are two types:
    • B Lymphocytes (B Cells): associated with humoral immunity e.g. involving antibodies present in body fluids, develop in bone marrow
    • T Lymphocytes (T Cells): associated with cell-mediated immunity e.g. involing body cells, developed in the thymus gland
  • Both are formed from stem cells found in bone marrow
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T cells and cell-mediated Immunity Continued

Cell-mediated Immunity

  • T lymphocytes respond to own cells that have been invaded by non-self
  • Also respond to transplanted material genetically different
  • T lymphocytes distinguish invader cells from normal because:
  • Phagocytes that engulfed and broken pathogens present some of pathogen's antigens on own cell surface membrane
  • Body cells invaded present viral antigens on own cell surface membrane as distress
  • Cancer cells present antigens on cell surface membrane
  • T Cells only respond to antigens attached to body cells: Cell-Mediated Immunity
  • In response of T Cells to infection by a pathogen:
    • Pathogens invade body cells or taken in by phagocytes
    • Phagocyte places antigens from pathogen on its cell surface membrane
    • Receptors on certain T helper cells fit exactly onto these antigens
    • This activates other T Cells to divide by mitosis and form a clone
    • Clone Cells: develop into memory cells for rapid response to future infections, cause phagocytes to engulf pathogens, stimulate B Cell division and kill infected cells
    • Role of receptors on T cells important as respond to single antigen
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T cells and cell-mediated Immunity Continued

How T Cells kill Infected Cells

  • By producing a protein that makes holes in the cell surface membrane
  • Cell becomes freely permeable to all substances so die
  • Action of T Cells is most effective against viruses because live inside cells
  • Viruses need living cells to reproduce, sacrifice of body cells prevents multiplying and infecting more cells
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6.4 B Cells and Humoral Immunity

Humoral Immunity

  • Involves antibodies which are soluble in the blood and tissue fluid (humour)
  • For each antigen there is a B Cell that has an antibody complementary
  • Antibody attaches to the complementary antigen
  • The B Cell divides by mitosis to form a clone which produces antibody specific to the foreign antigen
  • Typical pathogens have many proteins on their surface that act as antigens
  • Pathogens e.g. cholera produce toxins that act as antigens
  • Many B Cells produce clones with there own antibody type
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B Cells and Humoral Immunity Continued

  • For each clone they produce one of two cells:
  •  
    • Plasma Cells: secrete antibodies directly, survive only few days but make around 2000 antibodies every second. These antibodies destroy the pathogen and toxins produced, they are responsible for immediate defence: Primary Immune Response
  •  
    • Memory Cells: often live decade, don't produce antibodies directly but circulate in blood and tissue fluid. When encounter same antigen at later date divide rapidly and develop into plasma and more memory cells. Plasma cells produce antibodies needed to destroy pathogen, memory cells circulate in readiness for future infection. Memory cells provide long term immunity: Secondary Immune Response, it is more rapid and of greater intensity that primary
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B Cells and Humoral Immunity Continued

Summary of Role of B Cells

  • Surface antigens of invading pathogen taken up by B cells
  • B cells process antigens and present them on their surface
  • T helper cells attach to processed antigens on B cells thus activating them
  • B Cells activated to divide my mitosis to give clone of plasma cells
  • Cloned plasma cells produce antibodies that fit the antigens on pathogen's surface
  • Antibodies attach to antigens on pathogen and destroy: primary immune response
  • Some B cells develop into memory cells, can respond to future infections by same pathogen by dividing and developing into plasma cells that produce antibodies: secondary

Antigenic Variability

  • Pathogens which cause chickenpox are of a single type so are quickly identified by memory cells
  • Influenza has over 100 strains, its antigens are constantly changing: antigenic variability
  • Antigens won't correspond to the antibodies or memory cells from previous infections
  • To overcome the infection the primary response is used so is slower
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6.5 Antibodies

  • Are proteins synthesised by B cells
  • When the body is invaded B cells produce antibodies
  • Antibodies react with antigens on surface of the non-self material by binding to them
  • They are specific and there is a variety of them as they are made of proteins
  • Made up of four polypeptide chains, the chains of one pair are long (heavy chains) and the other chain is shorter (light chains)
  • To help the antibody fit around the antigens they change shape as though on hinge
  • Antibodies have binding sites that fit precisely onto antigens to form antigen-antibody complexes
  • The binding site is a variable region as it is different for each
  • Each site consists of a sequence of amino acids that form a 3D shape
  • The rest of the antibody is a constant region as it remains the same, it binds to receptors on cells such as B cells
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Antibodies Continued

Monoclonal Antibodies

  • Each antigen will induce a different B cell to multiply and clone itself
  • Each clone produces a different antibody collectively known as polyclonal antibodies
  • Monoclonal antibodies are antibodies that can be isolated and cloned as a single type
  • Monoclonal antibodies have useful functions:
  • Separation of a chemical from a mixture
  • Immunoassay: method of calculating amount of substance in a mixture e.g. pregnancy kits
  • Cancer treatment: can make the antibodies attach to cancer cells, used to activate a cytotoxic drug which destroys the cancer cells
  • Transplant surgery: transplanted organs suffer rejection due to action of T cells, monoclonal antibodies are used to knock out the T cells
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6.6 Vaccination

  • Immunity is ability to resist infection and takes two forms:
    • Passive immunity: produced by introduction of antibodies into individual from outside source, antibodies are not produced by self so are not replaced so immunity is short lived
    • Active immunity: produced by stimulating the production of antibodies by own immune system, generally long lived
  • Vaccination is the introduction of a substance of the best with intention to stimulate active immunity against a particular disease

Features of Successful Vaccination Programme

  • Suitable vaccine that is economically available in sufficient quantities
  • Few side effects, unpleasant side effects discourage individuals from use
  • Means of producing, storing and transporting the vaccine must be available which involves technology and good hygiene
  • Means of administering vaccine properly with trained staff
  • Be able to apply to majority, best done at the same time so pathogen transmission is interrupted: herd immunity
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Vaccination Continued

Why Vaccination does not Eliminate a Disease

  • It is difficult to eradicate a disease because:
  • Vaccination fails to induce immunity in certain individuals e.g. defective immune system
  • May develop disease immediately after the vaccination before immunity levels are high enough to prevent it
  • Pathogen may mutate so antigens change suddenly rather than gradually, vaccine becomes ineffective as new antigens on pathogen are not recognised by immune system. As a result the immune system doesn't produce antibodies to destroy pathogens. This antigenic variability happens with influenza so immunity is short lived
  • Maybe so many varieties that it is impossible to develop a vaccine that is effective
  • Certain pathogens 'hide' from body's immune system by concealing themselves inside cells or living in places out of reach
  • Individuals have objections to vaccinations for religious, ethical or medical reasons
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Vaccination Continued

Problem controlling Cholera and Tuberculosis by Vaccination

  • Cholera:
  • Is an intestinal disease so not easy to reach by immune system, oral treatment rarely has time to be effective as flushed from intestine by diarrhoea
  • The antigens of the cholera pathogen change rapidly making it difficult for lasting vaccine
  • Mobile populations from tourism and refugees spread cholera
  • TB:
  • Increase in HIV infection so more people with impaired immune systems
  • Poverty and wars created refugees often housed in overcrowded accommodation
  • Mobile populations from tourism and refugees spread TB
  • Elderly population is increasing who have weaker immune system
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