steps u need to rmb

• MAKING MABS

  1. A mouse is injected with antigen X 
  2. Activates B cells to produce antibodies against Antigen X (purify)
  3. Plasma B cells are taken from the Mouse's spleen 
  4. Mouse cells and myeloma cells are mixed together in culture medium, forming hybridoma cells 
  5. Hybridoma cells are cultured in new medium, where they grow and replicate 
  6. Hybridomas are screened for antibody production and cultured again to produce monoclonal antibodies 
• Steps in cell mediated immunity

  1. Antigen-presenting cells with foreign antigens on MHC-II markers bind to specific helper T cells in lymph nodes

  2. Helper T cells undergo clonal selection and expansion, forming effector and memory T cells

  3. Helper T cells secrete interleukins (cytokines) to stimulate immature T cells

  4. Immature cytotoxic T cells bind to self-cells with abnormal foreign MHC-I markers or APC displaying foreign antigens (MHC-II markers for APC, MHC-I for other infected cells)

  5. Cytokines from helper T cells stimulate cytotoxic T cells to proliferate, forming activated and memory cytotoxic T cells through clonal selection and expansion

  6. Cytotoxic T cells destroy infected cells through apoptosis
• STEPS IN HUMORAL ADAPTIVE IMMUNITY

  1. New antigen enters the body and reaches lymph nodes.
  2. It contacts many naïve B cells that don't recognize it.
  3. Eventually, it meets a B cell that recognizes and binds to it (clonal selection).
  4. Helper T cells bound to the antigen release cytokines to activate the correct B cells.
  5. Activated B cells differentiate and proliferate into plasma cells and memory B cells (clonal expansion).
  6. Plasma cells secrete antibodies against the specific antigen.
  7. Memory B cells remain in lymphoid tissue and respond rapidly upon re-exposure to the same antigen.
• Humoral = plasma b and memory b
• cell mediated = cytotoxic t cells, helper t cells and memory t cells
• Steps of inflammatory response

  1. Damaged cells release cytokines (chemokines) to signal to mast cells

  2. Mast cells release histamine

  3. Histamine causes nearby blood vessels to dilate and become more permeable (vasodilation)

  4. Blood flow to the damaged area increases and phagocytes are delivered to the site of infection (chemotaxis)

  5. Phagocytes are attracted to the area by cytokines and squeeze out of the blood vessels

  6. Phagocytes engulf bacteria, cell debris and pus by phagocytosis

  7. Platelets clot blood to stop the entrance of pathogens
• STAGES OF INFLAMMATION

  The inflammatory response can be divided into three main stages:

  • the vascular stage, which involves the actions of blood vessels
  • the cellular stage, which involves the actions of immune cells
  • the resolution stage, when inflammation is stopped and the normal state is restored.
• Steps in phagocytosis

  1. The pathogen is identified by a pattern recognition receptor (PRR) and engulfed by outfoldings of the plasma membrane of the phagocyte.
  2. The pathogen is engulfed in a vesicle called a phagosome.
  3. Lysosomes fuse with the phagosome (forming a phagolysosome).
  4. Toxic chemicals from the lysosome (include free radicals, lysozymes and proteases) digest and destroy the pathogen.
  5. Indigestible material is discharged from the phagocytic cell by a process of exocytosis.
• STEPS OF WHEN PATHOGEN ENTERS THE BODY

  1. Pathogen recognised by PRRs by surface detectors on phagocyte 
  2. Pathogen is engulfed in phagosome vesicle
  3. Lysosome fuses with a phagosome (phagolysosome) 
  4. Lysosomes enzymes break down and digest pathogen 
  5. Indigestible material is removed through exocytosis