3.2.4 Immune system

• Antigen- a glycoprotein/ glycolipid molecule on the cell surface which generates an immune response when detected by white blood cells
• Not recognised by the immune system due to foreign antigens:

  • Pathogens- foreign antigens on surface
  • Abnormal cells- abnormal surface antigens
  • Toxins- antigen molecules
  • Foreign cells- cells are the same species, but from another individual, so antigens will be different from host cell
• Phagocytes- white blood cells that engulf and destroy foreign particles, released in large amounts, produced in bone marrow
• Lysosomes- single membrane bound organelles, inactive hydrolytic enzymes (lysozymes) which activate when bound to other organelles
• Pathogens that invade the body may be engulfed by cells which carry out phagocytosis. The engulfed pathogen forms a vesicle known as a phagosome. Once engulfed, the pathogen is hydrolysed by enzymes called lysozymes, which are released from organelles called lysosomes.
• Antigen Presenting:

  • Phagocyte recognises foreign antigen on the pathogen
  • Phagocyte engulfs the pathogen and a phagosome is formed by a vesicle- contains pathogen
  • Lysosome fuses, forming a phagolysosome
  • Lysozymes (hydrolytic enzymes contained in lysosomes) hydrolyse pathogen
  • Antigens of the pathogen are stuck onto the surface membrane of the phagocyte to activate immune response
• Clonal Selection- T/ B cell carrying specific antigen receptors are stimulated to divide, forming clones
• Lymphocyte- a type of WBC which can mature to become B-lymphocytes or T-lymphocytes, produced in bone marrow
• Killer T-cells- secrete toxins when attached to pathogen to destroy their membrane
• Helper T cells- produce cytokines to stimulate B-cells to develop into plasma cells to make antibodies
• Antibodies- produced by B-lymphocytes, binds to specific antigens to signal the immune response, many RER, many mitochondria, many ribosomes, larger golgi body
• Structure of antibodies- variable region, antigen binding site, disulphide bridges, constant region, hinge region
• Agglutination- clumping of antibodies onto multiple antigens to form a clump of pathogens, aiding phagocytosis
• Opsonization- antibodies attach to pathogen, making them more visible to phagocytes
• Antigen Variation- changes in the external structure of the two antigen types, due to mutations in nucleic acid
• Genetic Shift- complete change in virus structure
• Genetic Drift- slow change in structure of virus, however some similarities remain
• Reassortment of genetic material: exposure to different strains of virus leads to mixing of antigens and genetic material within an infected cell, making a new strain
• Vaccines can be made from:

  • dead/ inactive pathogens- has antigens, no virulence so no disease caused
  • weakened, live form of pathogens- can't replicate, no disease caused
  • substances from parts of pathogen/ toxin- antibodies can be made, faster response
  • particular protein/ small fragment of pathogens- antibodies can be made so better immune response
• Monovalent vaccine- immunises against a single antigen/ strain of pathogen
• Multivalent vaccine- immunises against multiple antigens/ strains of pathogen
• Vaccines act as a primary infection so memory cells can be produced, meaning the secondary infection is less severe due to a faster, secondary immune response
• Pathogen- an organism which can cause disease
• HIV (human immunodeficiency virus) and AIDS (acquired immune deficiency syndrome)- virus attacks the immune system, causing an infected person to be more vulnerable to opportunistic diseases
• Structure of HIV:

  • Genetic material- RNA (single stranded)
  • Capsid- surrounds RNA
  • Lipid membrane
  • Attachment proteins
  • Reverse transcriptase (enzyme)
• Life cycle of HIV:

  • HIV's attachment proteins bind to receptors on helper T-cell surface.
  • Membrane of HIV virus fuses with helper T-cell membrane, contents of virus released into helper T-cell.
  • Enzyme reverse transcriptase converts RNA into DNA.
  • HIV's DNA is inserted into helper T-cell's DNA and transcribed into HIV mRNA.
  • HIV mRNA is translated into new HIV proteins.
  • New HIV particles are assembled and leave the helper T-cell with a lipid envelope from the helper T-cell’s membrane.
• Normal immune response:

  • Pathogen enters
  • Helper T-cells stimulate other T-cells and B-lymphocytes
  • Cell/ antibody mediated response
  • Pathogen destroyed
• HIV-infected immune response:

  • Pathogen enters
  • T-cells infected by HIV
  • More HIV produced and released, HIV goes on to infect other helper T-cells
  • Less immune response, so no destruction of pathogen
  • Opportunistic infection
• Latency period- HIV replication drops to a low level and the infected person might not develop symptoms for many years
• Role of the disulphide bridge in forming the quaternary structure of an antibody- holds together the two polypeptide chains to prevent them from separating
• Explain how HIV affects the production of antibodies when aids develops in a person (3 marks):

  Less antibodies are produced (1), because HIV destroys helper T-cells (2), so less B-cells are able to be stimulated into differentiating into plasma cells (3).
• Explain how determining the genome of the virus could allow scientists to develop a vaccine (2 marks):

  The scientists could identify proteins that come from the genetic code (1), and could then identify antigens which they could use in the vaccine (2).
• Describe how B-lymphocytes would react to vaccination (3 marks):

  The B-cell binds to the complementary antigen (1). Plasma cells produce antibodies against the virus (2), and develop memory cells (3).
• Monoclonal antibody- an antibody which is produced from identical plasma cells
• Uses of monoclonal antibodies in medical treatment:

  • Targets specific cells
  • Carries drugs to specific cells
  • Blocks antigens on specific cells
• Uses of monoclonal antibodies in medical diagnosis:

  • Pregnancy tests
  • ELISA tests
• Finding results in an ELISA test:

  • First antibody binds to it's complementary antigen.
  • Beaker is rinsed to remove any antibodies which did not attach.
  • Second antibody with enzyme attached to it is added.
  • Beaker is rinsed again.
  • If the second antibody with the enzyme attaches to the first antibody-antigen complex, when the substrate is added, the colour will change, indicating a positive test.
  • If the colour does not change, this indicates a negative test since the second antibody did not attach to the first antibody, meaning the first antibody did not bind, and was therefore washed away.
• How vaccination works to create a faster secondary reaction:

  • Antigen on the surface of pathogen binds to receptor on the surface of a T-cell.
  • T-cell is activated and releases cytokines.
  • Cytokines released by the T-cell stimulate the production of plasma cells.
  • Plasma cells release antibodies.
  • Some B-cells become memory cells.
  • Memory cells produce antibodies faster in the case of a secondary infection, leading to less illness caused.
• Describe how vaccines lead to the production of antibodies against a pathogen (5 marks):

  Vaccine contains an antigen from a pathogen (1), macrophage presents antigen on it's surface (2), T-cell with a complementary receptor protein binds to the antigen (3) and the T-cell stimulates a B-cell with a complimentary antibody on it's surface (4). The B-cell produces large amounts of antibodies and divides to form clones which all produce the same antibody (5).