Immunology

• Immune system = system that protects body against infection
• Immunity = ability to defend against infection/pathogen  immune cells must be able to differentiate between foreign cells and own cells (as well as altered self cells e.g. cancer cells)
• Antigen = a molecule that elicits an immune response (so any molecule that is recognised and elicits an immune response)
• What are the four features of the immune system - specificity, diversity, memory, tolerance
• What are the three types of immunity: mechanical/chemical, innate, adaptive
• Cytokines: Small protein that induces a signalling response (in neighbouring cells)
• white blood cell - cell types = lymphocytes, monocytes, eosinophils, basophils, neutrophils
• example of PRRs = Toll like receptors
• Activation of PRRs result in upregulation of co-stimulatory molecule tells body that there is something to react to
• Phagocytes = neutrophils, macrophage, dendritic
• Antigen presenting cells = macrophages, dendritic cells
• NK cells kill virally infected cells
• Interferons(type of cytokine) inhibit viral replication
• How NK kills: Perforin creates pores in membrane, granzyme induces apoptosis of target cell
• How do we recognise virally infected cells: downregulate MHC Class I and stress response
• 3 modes of activation of complement system: classical, mannose binding lectin, alternate
• 3 methods of complement: cleavage products (C3a, C5a) are potent chemoattractants (attract immune cels), MAC complex, optimisation of bacteria
• What are the types of defenses: physical barrier, chemical defences/barriers (AMPs, cytokines), inante immune system (cellular responses - phagocytes, complement), adaptive immune system (B cells and T cells)
• when does the adaptive immune system kick in: after 96 hours
• The chaperones involved in MHC Class I in ER are ERP57 and calreticulun
• an example of viral protein interfering with MHC Class I pathway: Viral evasins U26 prevent peptide movement through TAP
• signals that act as stop signals for CTL: CTLA4 which bind CD80 and CD86 and stop signalling, as well as PD-1 that binds PD-L1
• immunological memory is:

  • Rapid, effective response to remove pathogen that differs qualitatively from primary response (faster and bigger
• ELISA is:  enzyme-linked immunosorbent assay
• What are the 3 functions of anitbodies: neutralisation, opsonisation and complement activation
• What is opsonisation?

  • Antibody promotes phagocytosis as B-cell receptor constant domain binds on receptor on phagocytes and gets internalised, and bacteria and pathogen gets broken down. The other part will be binding the virus/bacteria. 
• passive immunity:

  • Transfer of antibodies from a person or animal who has recovered from the disease – training own cells to produce antibodies (cells will provide memory of that antibody when exposed)
• active immunity: When exposure to a disease results in an immune response (within body) that leads to antibody production (antivenom = example)
• immune in subsequent infections: bigger and faster
• vaccines: exposure to antigenic material (that is incapable of causing disease) to induce immune response and generate memory cells by mimicking the first infection