AQA Biology Unit 1.6. Immunity


  • 6.1 Defence Mechanisms
  • 6.2 Phagocytosis
  • 6.3 T cells and cell-mediated immunity
  • 6.4 B cells and humoral immunity
  • 6.5 Antibodies
  • 6.6 Vaccination
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6.1 Defence Mechanisms

Defence Mechanisms: Protect us from pathogens which cause disease; this is either from secretion of harmful toxins or from infecting and damaging host cells.

Non-specific: Mechanisms that do not distinguish from one type of pathogen from another, so responds to all in the same way. These include barriers to entry of pathogens and phagocytosis and respond rapidly. Example of barriers:

  • Skin - provides a physical barrier that pathogens cannon penetrate.
  • Epithelia covered in mucus - goblet cells secrete mucus, pathogens stick to mucus, cilia move pathogens up trachea to be swallowed into stomach.
  • Hydrochloric acid in stomach - Low PH denatures enzymes of pathogens, leading to pathogens being destroyed.

Specific: Mechanisms that do distinguish from one type of pathogen from another. The responces are less rapid but give long-lasting immuniy. This comes in the form of: cell-mediated responses involving T-cells and humoral responses involving B-cells.

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6.2 Phagocytosis

Phagocytosis: A non specific mechanism that responds rapidly to infection from pathogens. Phagocytosis involves phagocytes (a type of white blood cell) and the process is as follows:

  • Histamine is released causing dilation of blood vessels speeding up arrival of phagocytes to the site of infection.
  • Phagocytes attracted by toxins/chemicals pathogen secretes known as chemoattractants and attach themselves to surface of pathogen.
  • Phagocytes form a gulf around pathogen and then engulfs the pathogen.
  • Part of cell-surface membrane of phagocyte is used to contain ingested pathogen within a phagosome.
  • Lysosomes migrate towards phagosome and release their lytic enzymes.
  • Lytic enzymes hydrolyse,destroy and digest pathogen of which soluble products are absorbed into the cytoplasm of phagocyte.

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6.3 T cells and cell-mediated immunity

Antigens: A protein that is recognised as non-self stimulating an immune responce. This stimulates the production of antibodies.

T Lymphocytes: Mature in Thymus gland and associated with cell-mediated immunity.

Cell-mediated immunity: A specific mechanism where T-lymphocytes respond to antigen-presenting cells.

  • Pathogen invade body cells or taken in by phagocytes.
  • Antigens from pathogen displayed on cell surface membrane.
  • Receptors on certain T-cells fit exactly onto antigens.
  • Activates T-cells to divide rapidly by mitosis and form a clone.
  • The cloned T cells : (a) Develop into shape-memory cells for rapid responce to future infections by same pathogen (b) Stimulate phagocytes to engulf pathogens by phagocytosis (c) stimulate B-cells to divide (d) Kill infected cells.
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6.4 B cells and humoral immunity

B-Lymphocytes: Mature in Bone marrow and involved in humoral immunity.

Humoral Immunity: A specific mechanism where antigen presenting B-cells are activated by t-cells to carry out humoral immunity and the process is as follows:

  • Antigens on surface of pathogen is taken up by B-cells.
  • B cells process the antigen and present them on their surface.
  • T-helper cells attach to the displayed antigen on B-cells activating the B-cells.
  • B-cells activiated to divide by mitosis to give a clone of plasma cells.
  • Cloned plasma cells produce antibodies that are specific to the shape of antigens on pathogen's surface.
  • Primary immune responce is that antibodies attach or bind to antigen on pathogen forming an antigen-anitbody-complex, destroying pathogen.
  • Secondary responce is a result of some B-cells developing into shape memory cells. Divides rapidly into plasma cells that produce antibodies.
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6.5 Antibodies

Antigenic Variability: Describes the shape of antigens of a pathogen as constantly changing. Thesefore new strain causes disease as antibodies from previouse infection do not compliment shape of antigen of the new strain. Cannot respond to infection by secondary responce, so must use primary responce.

Antibodies: Synthesised by B-cells, and are very specific in shape to bind to a specific antigen shape. Antibodies are made up of four polypeptide chains so is a quaternary structure. Antibodies bind to complimentary antigen to form an antigen-antibody-complex Antibodies have a variable region, made up of a speicific sequence of amino acids that make up the 3-D tertiary shape. Also has a constant region that is the same in all antibodies that bonds to receptors on B-cells.

Monoclonal Antibodies: The cloning of a single type of antibody outside of the body. Can be used in cancer treatment, transplant surgery, imunoassay and sepearation of a chemical from a mixture.

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6.6 Vaccination

Vaccination: Injecting an individual with a weakened/attenuated form of a pathogen containing the antigen of a pathogen that stimulates an immune responce. This stimulates production of shape-memory cells. This gives immunity to pathogen as shape memory cells divide rapidly during secondary infection to produce antibodies that bind to pathogen antigen and destroys them before pathogen causes disease.

Passive Immunity: Produced by introduction of antibodies to individuals from an outside source, therefore not replaced by individual and eventually broken down by body. Generally short-lived.

Active Immunity: Stimulating production of antibodies by individuals own immune system. Generally long-lasting.

Successful Vaccination Programme: Economically viable, few side-effects, herd immunity, means of administering vaccine, means of producing/transporting/storing vaccine.

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6.6 Vaccination

Why vaccination does not eliminate disease: Fails to induce immunity in people with defective immune systems. May develop disease immediately after vaccination but before immunity levels are high enough to prevent infection. Mutations of pathogen causes antigenic variability e.g. influenza changes its antigen shape frequently. Many strains of a particular pathogen so cannot develop vaccine against all. Individuals object to vaccination.

Problems with controlling cholera:

  • Intestinal disease so not easily reached by immune system or antibiotics.
  • Antigen of cholera pathogen changes rapidly (antigenic variability).
  • Mobile populations spread cholera.

Problems with controlling TB:

  • Increase in HIV infection so more people with impaired immune systems.
  • Poverty, wars, political unrest create breeding grounds for TB e.g. refugee camps.
  • Proportion of elderly people in population increasing, as these people have a less effective or weakened immune system.
  • Mobile populations so difficult to ensure individuals are vaccinated.
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This was soooooooo helpful!! Thank you so much for posting this.

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