cell recognition and immune system

• at several points in the mitotic cell cycle a checkpoint operates , cell cycle checkpoints are regulated by cell-signalling proteins
• cell cycle checkpoints

  • G1 checkpoint : 2 features are checked

  1. whether conditions are appropriate for proceeding with the cell cycle
  2. dna damage

  • also contains a special checkpoint called the restriction point - the point at which the cell irreversibly commits to entering the cycle
• cell cycle checkpoints

  • G2/M checkpoint:
  • cell ensures all the chromosomes have replicated properly
• cell cycle checkpoints:

  • metaphase / spindle checkpoints
  • ensures the cell cycle will not proceed until all the sister chromatids are properly attached to the mitotic spindle
• normal cells reproduce and stop when there are enough whereas cancer cells continue to multiply indefinitely
• normal cells bind to form tissues whereas cancer cells detach from neighbouring cells and spread quickly
• normal cells have programmed cell death ( apoptis ) if damaged whereas cancer cells are mutated and do not respond to normal cell signalling
• normal cells become specialised or mature , cancer cells remain immature
• cell divisions

  • mechanisms controlling division are not perfect
  • genes controlling it might mutate or cells go into the cell cycle unnecessarily
  • usually these cells are destroyed by white blood cells
  • if the protective mechanism breaks down and cells remain in cycle , tumour can form
• mestasised is when a tumour or cancer has spread to another organ
• genes behind cancer

  • oncogenes : genes which normally function as to promote appropriate cell growth ( activated in cancer )
  • tumour suppressor gene : genes that normaly function to stop inappropriate cell growth ( prevent cancer )
• oncogenes:

  • codes for proteins that stimulate the cell cycle
  • if one of these genes mutate it causes those genes to be continually active
  • so the cell cycle is continually stimulated so cells divide uncontrollably causing cancer
• tumour suppressor cells:

  • normally produces chemicals that suppresses the cell cycle
  • mutations in these genes results in uncontrolled growth
  • this stops transitions between G1 and S
  • a mutated p53 protein wont work properly
• how do we treat cancer?

  • prevent dna from replicating
  • inhibit metaphase stage of mitosis by interfering with spindle fibre formation
  • but treatment doesnt only effect cancer cells but may cause hair loss
• label the antibody

  A) antigen binding sites

  B) variable region

  C) light chain

  D) heavy chain

  E) constant region

  F) receptor binding site

  
• what are the two types of targeted medication?

  direct monoclonal antibody therapy and indirect monoclonal antibody therapy
• becuase viruses live inside of host cells and because they dont have cell walls, antibiotics dont work on them
• HIV structure

  • core - contains genetic material (rna in hiv) and enzyme reverse transcriptase
  • capsid- outer protein coat
  • envelope- extra outer layer made of membrane from the host cells membrane with protein attachments on the exterior to enable it to attach to the hosts helper t-cells
• replication of HIV in helper t-cells:

  1. HIV is transported in the blood until it attached to a CD4 protein on a helper t-cell
  2. the HIV protein capsule then fuses with the helper t-cells membrane enabling RNA and enzymes from the HIV to enter
  3. HIV enzyme reverse transcriptase copies the viral RNA into a DNA copy and moves to the helper t-cells nucleus
  4. this is why its called a retrovirus
  5. here mRNA is transcribed and the helper t-cells start to make viral proteins to make new virus particles
  6. this destroys the helper t-cells causing flu-like symptoms
• how does HIV replicate (4 marks)

  1. attachment proteins attach to receptors on helper t-cells
  2. RNA/nucleic acid enters the cell
  3. reverse transcriptase converts RNA to DNA
  4. viral protein/capsid/enzymes are produced
  5. virus is assembled and released from the cell
• describe phagocytosis?

  • phagocyte is attracted to a pathogen by the chemical products released by it, it moves along the concentration gradient
  • the phagocyte has several receptors on the surface that binds to the chemicals on the surface of the pathogen
  • a phagosome is formed when the phagocyte egulfs the pathogen and lysosomes within the phagocyte moves towards it
  • lysosomes releases lysozymes into phagsome
  • the hydrolosis products of the bacterium is absorbed by the phagocyte
• what do lymphoctyes do?

  identify non-self cells and destroy or neutralise them
• how are non-self cells identified?

  cells have specific molecules on its surface which are likely to be protein molecules due to the unique 3d structure
• what is an antigen?

  generates immune responses by triggering lymphoctyes, they are usually proteins on the surface of a cell
• how do antigens variate ?

  pathogens DNA mutate frequently, this may change the shape of antigens so previous immunity will no longer be effective
• what are the types of immune responses?

  • 1st line of defence : chemical or physical
  • 2nd line of defence : immune system ( white blood cells)
• what is used for specific and non-specific responces?

  phagocytes: non-specific and lymphocytes: specific
• where a phagocytes found?

  in the blood and tissue
• what type of white blood cell is a phagocyte?

  macrophage
• what are the two lymphocytes?

  t-cells and b-cells
• where are all lymphocytes produced?

  bone marrow
• where do t-cells mature?

  thymus gland
• what response is involved with t-cells?

  cell-mediated response
• what is an antigen presenting cell?

  when a cell had been engulfed by a phagocyte and hydrolysed the antigens are put on the surface of the pathogen
• what are cytotoxic t-cells and how do they work?

  • cells that kill/destroy pathogens by releasing a protein called perforin that embeds to make holes in the cell membrane
• describe the cell mediated response?

  • pathogens invade body cells or are taken in by phagocytosis
  • the phagocyte places antigens from the pathogen on its cell surface membrane
  • receptors on a specific helper t cell fit exactly onto these antigens
  • this attachment activates the t cell to divide rapidly by mitosis and form a clone of genetically identical t cells
  • the cloned t cells:

  1. stimulate phagocytes to engulf pathogens
  2. develop memory cells
  3. stimulates b cells to divide and secrete their antibodies
  4. activate cytotoxic t cells
• where are b-cells made and where do they mature?

  bone marrow
• what response are b-cells involved in?

  humoral immunity
• why is it called a humoural response?

  because antibodies are soluble and transported in bodily fluids and 'humor' is an old term for body fluids
• how many different b-cells are there?

  10 million