Immunity

• phagocytes recognise pathogens from the pathogens foreign antigens on the membrane
• During phagocytosis, phagocytes are attracted to pathogens by chemotaxis, pathogen is recognised by antigens then engulfed by phagocyte and dragged into a phagosome, then lysosomes containing hydrolytic enzymes fuse with phagosome to form a phagolysosome, pathogen is digested by the cell.
• Antibodies are only specific against specific pathogens because antibodies have a specific tertiary structure which is only complementry to a certain antigen and therefore can only destroy specific pathogens
• lymphocytes are smaller than phagocytes with a large nucleus, they can become B or T lymphocytes
• T-lymphocytes have cell surface receptors like antibodies and when they respond to antigens they can divide rapidly. they can develop into t killer or t helper cells
• T killer cells recognise antigens and attach to the pathogen then secrete a toxic substance to destroy its cell membrane
• T helper cells release cytokines that stimulate B cells development into plasma cells to produce antibodies
• Clonal selection- a T or B cell carrying a receptors that is specific for a particular antigen is stimulated to form a clone
• T helper cells make phagocytes more active and therefore makes phagocytosis more efficient
• T memory cells will divide into the correct T helper cells when required
• B lymphocytes have a surface covered in antibodies which can bind to antigens
• B lymphocytes differentiate into plasma cells when stimulated by the T helper cells
• Antibodies are Y shaped proteins with two binding sites on their tips
• When a B cell becomes a plasma cell it has more rough endoplasmic reticulum, ribosomes, mitochondria and Golgi body
• The structure of an antibody is a y shaped globular protein
• Each arm of the Y shape of an antibody contains variable regions that determine its specificity
• Agglutination sticks bacteria together, making it easier for the phagocyte to engulf many at once
• HIV virus contains a capsid, lipid envelop, attachment protein, rna, reverse transcriptase
• Inactivated vaccines contain dead or damaged pathogens which cannot reproduce but still trigger an immune response
• Outline the process of the cell-mediated response?

  • Complementary T helper cells bind to foreign antigen on APC.
  • Release cytokines that stimulate:clonal expansion of complementary T helper cells : become memory cells or trigger humoral response.
  • clonal expansion of T killer cells : secrete enzymes to destroy infected cells.
• Explain how antigen variability can be caused?

  mutation in DNA base sequences leads t a different sequence of codons in mRNA, changing the primary structure
• what are the 2 types of specific immune response:

  • humoral
  • cell-mediated
• antigen variability can be caused by mutations in the dna/rna or by reassortment of genetic info inside host cell (caused by infection of more than 1 strain)
• 1. Helper T cells (TH cells)

  These cells have receptors on their cell-surface that bind to complementary antigens on antigen-presenting cells. After binding, they can form memory cells, stimulate B cells or phagocytes, and activate cytotoxic T cells. 
• 1. Cytotoxic T cells (TC cells)

  These cells kill abnormal and foreign cells by producing a protein known as perforin. This protein makes holes in the cell-surface membrane, causing it to become freely permeable and causing cell death. 
• 1. Memory T cells 

  These cells provide long-term immunity against specific pathogens. They provide a rapid response if the body is re-infected by the same pathogen. 
• Primary immune response:

  1. The production of antibodies is slow after the first exposure to the pathogen (longer lag phase). 
  2. The concentration of antibodies increases slowly. 
  3. This is because there are very few B cells that are specific to the pathogen's antigens. 
  4. It takes time for the B cells to divide into plasma cells to produce the correct antibody, so the individual experiences symptoms of the disease. 
  5. During this process, some B cells divide into memory cells to make the individual immune to this disease.
• Secondary immune response:

  1. The production of antibodies is much quicker after exposure to the pathogen (shorter lag phase).
  2. The concentration of antibodies increases quickly. 
  3. This is because memory cells recognise the pathogen's antigens and quickly divide into plasma cells. 
  4. These plasma cells secrete larger numbers of antibodies to quickly destroy the pathogen before the individual experiences any symptoms.