AGR3AH Immunology Exam Preparation

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AGR3AH Immunology Exam Preparation
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  1. How does a symptom differ from a sign?
    • Symptom: something that is felt, or inward. A vet can’t see it for themselves. Doctors are told by the patient what the problem is, but vets aren’t so they have to work it out for themselves!
    • Sign: something that is observed, e.g a bruise, cut, flushed face etc
  2. What are the general signs of illness?
    • Not interested in food/vomiting
    • Not bright and alert
    • Coat and skin looking rough or hair/wool/feathers/scale loss
    • Faeces colour content, diarrhea, constipation
    • Other signs such as lameness, gait stiffness, swelling, bleeding, open wounds, fever, fits, foaming, pale membranes, unconscious, lesions, emaciation
  3. What are the factors influencing illness?
    • Host characteristics eg anatomy, sex, age, genetics, nutrition, stress levels, immune competence
    • Environmental factors (causes - nutrition, mechanical (cut gets infected)/thermal (overheat and get heat stress) injury, toxins) and affect on pathogens (temperature, humidity, degree of moisture in environment, grazing characteristics, prevailing wind direction, population density)
    • Mode of transmission (direct - droplet or aerosol, oral, contact; or indirect - foodborne, waterborne, vectorborne, fomite (bedding or things that the animal comes into contact with, that is passed on when another comes into contact with the object), environmental)
    • Human influences - on nutrition (over/under feeding), environment (improper housing), physical (inury or overcrowding), transportation (strees, hygiene), genetics (in-breeding)
  4. What is phagocytosis
    Where one cell can engulf organic material and/or whole cells, break it down and then expel the broken down contents
  5. What are the two types of immune mechanisms?
    • Soluble factors (Humoral immune response - when antibodies are produced)
    • Immune cells (Cell-mediated immune response)
  6. What are the two types of immune responses?
    • Innate: Non-specific recognition. No memory of previous assaults. First line of defence. Fast acting. Stops most potential threats. Present at birth.
    • Adaptive (Acquired): Specific recognition. Memory of previous response. Slower and more powerful in attacking the antigen. Develops over time (mostly).
  7. What are the 6 steps in phagocytosis?
    • Pseudopodia surround microbes
    • Microbes are engulfed into cell
    • Vacuole/phagosome containing microbes forms
    • Vacuole and lysosome fuse to become a phagolysosome
    • Toxic compounds and lysosomal enzymes destroy microbes
    • Microbial debris is released by exocytosis
  8. What are the roles of macrophages in the immune response?
    • Inflammation and fever
    • Lymphocyte activation
    • Tissue reoganisation
    • Tissue damage
    • Microbiocidal activity
    • Tumouricidal activity
  9. What is vasodilation?
    Expansion of veins/capillaries to increase capillary permeability
  10. What is chemotaxis?
    The process involving macrophages and neutrophils that causes attraction of phagocytes to infection site
  11. What is extravasation?
    Phagocytes migrate capillaries to site of tissue damage
  12. What are the two distinct phases of the inflammatory barrier?
    • Acute: Pain, swelling, heat, redness, loss of movement/function. Vasodilation, oedema (build up of fluid)
    • Chronic: 24-48hrs. Monocytes need to go through activation to become macrophages.
  13. What are the two types of antibodies?
    • B cells - surface bound antibody that binds to the b cell receptor
    • Plasma cells - secrete antibody free into the serum
  14. How can you test for antibodies/antigens?
    • Radioimmunoassays
    • Protein A/G or Strepavidin/Biotin binding
    • Enzyme-linked Immunosorbent Assays (ELISAs)
    • Western Blot
    • Immunoprecipitation assays
    • Fluorescence immunoassays
  15. How are ELISA's conducted?
    • Indirect ELISA method: Antigen coated on a plate. Antibody added (1st Ab). Labelled secondary (2nd) Antibody (binds to 1st Ab) (DIRECT SKIPS THIS STEP). Chromogenic substrate added. Optical Density measured.
    • Sandwhich ELISA: Developed antibody that binds to antigen, this is added to the plate, followed by the antigen, and then the antibody again, then add antibody with label, then substrate added, then measure OD
  16. Lymphoid cells and myeloid cells are collectively known as what?
    Leukocytes/White blood cells
  17. What CDs are expressed by which cells?
    • All T cells – CD3+, CD28+, CD45+
    • T helper cells – CD4+
    • T cytotoxic cells – CD8+
    • Treg cells CD4, CD25 (majority)
    • Natural killer cell – CD16+, CD56+, CD3-
    • B cells - CD19, CD 20, CD40
    • Macrophages - CD1a-c, CD11b, CD40, CD64
    • Dendritic cells - CD1a-e, CD35, CD40
    • NB: ‘+’ expressed by cell, ‘-’ not expressed by cells
  18. What are the 3 types of T cells?
    • T Helper (Th) cells: Express CD4 – recognise MHC Class II. Help B cells divide, differentiate & produce ab. Can be further divided into Th1 and Th2 cells.
    • T cytotoxic (Tc) cells: Express CD8 – recognise MHC Class I. Bind & kill pathogens & infected/cancer cells.
    • Regulatory T (T reg) cells:Suppress T & B cell activity
  19. What are the characteristics of a B cell?
    Develop in bone marrow. CD19, CD20, CD21. Express surface immunoglobulin (Ig) - Antigen receptor. Most divide and differentiate into plasma cells which secrete Ig. Some become memory cells, which have high affinity surface Ig, recognise repeat antigen and increase in numbers for stronger attack (Clonal expansion).
  20. What are plasma cells?
    • Differentiated B cells:
    • ↑ endoplasmic reticulum (ER) & Golgi apparatus
    • Secrete ↑ Ig
    • Last days-months
    • No longer APCs (lack MHC Class II)
    • Important for Humoral Immunity (antibodies)
    • Cannot switch Ig class once differentiated from B cells
    • Produce high affinity Ig
    • Found in bone marrow (long lived plasma cells) and secondary lymphoid organs (spleen, lymph nodes)
  21. What are Null cells?
    Non-T/Non-B Cells that don’t express CDs found on B or T cells. Lack conventional antigen receptors. Go through differentiation to become NK cells
  22. What are NK cells?
    • CD16, CD56 (CD3-)
    • Kill virally infected cells/cells that have lost MHC Class I expression
    • 2nd line of defence against viruses (get what Tc cells miss)
    • Similar mechanisms to Tc cells - granules (perforin & granzymes)
  23. What are granulocytes?
    A type of myeloid cell that attacks other cells. 4 types (eosinphils, neturophils, basophils and mast cells).
  24. What are the 3 roles of macrophages?
    Tissue repair, inflammatory response (chronic) and adaptive immunity activation (APCs)
  25. What granulocyte is first at the inflammation site?
    Neutrophils
  26. What is the role of Eosinophils?
    • Release granules: Tissue destroying & Anti-parasitic, Acidic, Crystal structure, Suppress inflammation (E.g. histaminase)
    • Can be phagocytic but main function is exocytosis (release granules)
  27. What are platelets?
    • Anuclear
    • React with Fibrinogen
    • Clot to prevent blood loss
    • Modulate inflammation
  28. What are the primary and secondary lymphoid organs?
    • Primary (immune cell production): Bone marrow (humans, rodents and all others)/ileal Peyer’s patches (ruminants and dogs)/Bursa of Fabricius (birds) and Thymus
    • Secondary (cell storage and antigen contact): Lymph nodes, spleen and mucosal associated lymphoid tissue
  29. What happens in the bone marrow?
    • Early cell differentiation in all animals (haemopoietic stem cells): T cell precursors and B cell precursors
    • B cell maturation in Rabbits, Rodents and Humans
  30. What is the bursa of fabricius?
    A lymphoepithelial organ located in the Cloaca/intestine, it is the site of Maturation of B cells. It is Larger in young birds
  31. What are Ileal Peyer's patches?
    • Organised lymphoid nodules in the Intestinal tract (ileum) with a Thickened epithelium. It is the site of B cell maturation in ruminants, pigs, dogs
    • Happens in germinal centres
  32. What is the thymus?
    The site of T cell maturation, after T-cell precursors have migrated to here. The thymus selects cells that can distinguish self and foreign proteins, those cells that cannot distinguish are destroyed. The thymus is made up of lobules, with the outer cortex containing rapidly dividing pre-T cells and the inner medulla containing mature T cells and APCs.
  33. What is lymph?
    Circulating institial fluid that transports immune cells and antigens from body tissues to the lymph nodes (which filter lymph fluid are is the site of antigen/immune cell interaction). It is connected to the blood supply.
  34. What is the spleen?
    A secondary lymphoid organ that is made up of red pulp (destruction of old red blood cells and storage of current red blood cells) and white pulp (the peri-arteriolar lymphoid sheath - T and B cells, which doesnt not have lymph supply)
  35. What is Mucosal Associated Lymphoid Tissue (MALT)
    Tonsils, Peyer's patches, appendix, small aggregates of lymphoid tissue found in mucosal tissues. It diffuses aggregates of lymphoid tissue and is the main entry point of pathogens.
  36. What is the immune cell circulation pattern?
    Development in Bone Marrow then enter blood. Lymphocyte circulation/recirculation through blood and lymph. Increased chance of antigens to contact specific lymphocytes. Lymphocytes leave the lymph node and go to specific tissues, E.g. gut, skin, lung.
  37. What is haematopoiesis?
    Blood cell differentiation into lymphoid, myeloid and red blood cells that occurs in the bone marrow. Recognition and attack cells.
  38. What are the general functions of immunoglobulin?
    • Generation of oxidents
    • Immunoglobulin
    • Opsinisation
    • Activation of complement
    • Virus and toxin neutralisation
    • Antibody-dependent cell cytotoxicity (ADCC)
    • Direct anti-microbial activity
    • Reduced damage to host from inflammatory response
  39. What is the nature of the antigen-antibody interaction?
    • Lock and key concept: antibody-antigen complex. Compatibility.
    • Non-covalent bonds: overall strength (affinity)
    • Reversability: bonds can be broken
    • Occurs in the Fab region: Antibody paratope binds to antigenic epitope
  40. What is avidity?
    Affinity x number of binding sides
  41. What is cross reactivity and why is it important?
    • Ab recognises more than one antigen based on specificity and structure:
    • Same antigen, different pathogen
    • Similar antigen, different pathogen
    • Similar antigen, same pathogen (isomer)
    • Important because it can be used in immunisations to protect against multiple pathogens
  42. What is the mechanism of antibody formation?
    • Antigen encounter with a B cell (primed)
    • Activation of the Th cell (APC)
    • B cell activation by Th cell
  43. What does the Clonal Selection Model (Burnett 1959) say?
    • Each B cell - one type of antibody
    • Each B cell will place the antibody it makes into its cell membrane with antigen-binding side outward
    • Only B cells that bind to the antigen can complete their development into antibody-secreting plasma cell
    • The specificity of the antibody is exactly the same as that which was on the cell surface of the B cells
  44. How are monoclonal antibodies produced?
    • Vaccinate animal
    • Collect spleen cells
    • Fuse cells with myeloma cells - if they fuse the cells will survive
    • Select clonal population of B cells
    • Clone and purify monoclonal antibody
  45. What are the main antibody classes that are transferred to neonates in pigs/humans, and cattle/sheep
    • IgA in pigs and humans
    • IgG in cattle and sheep
  46. What is a nanobody?
    • The VH aka VHH aka V-NAR fragment of the Heavy chain antibody (VHH = variable domain of heavy chain of heavy-chain antibody)
    • Found in camelids and sharks
  47. What are the key properties of nanobodies?
    • Like normal antibodies, Nanobodies show:
    • - high solubility
    • - high target specificity
    • - high affinity for their target
    • - low inherent toxicity
    • However, like small molecule drugs, they:
    • - inhibit enzymes
    • - rapid tissue penetration
    • - access receptor clefts, which is challenging with normal antibodies
    • - think of the nanobody as a drug
    • Furthermore, Nanobodies:
    • - are generally very stable
    • - easily produced in recombinant form
    • - recognize hidden antigenic sites
    • - can be administered by means other than injection
    • - are easy to manufacture
  48. What are the uses of nanobody technologies?
    Anti- fungal, viral, venom, inflammatory, cancer
  49. How can nanobodies be used into treatment of trypanosomes?
    Use NbAn33 to deliver the apoL-1 toxin to the trypanosome, as Apolipoprotein A1 in human serum or as a nanobody toxin is lytic for trypanosomes
  50. What are the four types of tissue grafts, and what determines their success?
    • Autografts: Same individual, different site
    • Isografts: Between genetically identical individuals
    • Allografts: Closly matched, genetically dissimilar individuals – same species
    • Xenografts: From one species to another
    • Success is dependent on ‘tissue type’ and immunological acceptance by Major Histocompatibility complexes (MHC - donor and recipient must have the same). Skin biopsy from mouse genotype A can be given to another type A. Skin biopsy from mouse type B is rejected by type A, due to passenger leukocytes
  51. How can tolerance of tissue grafts be induced?
    • Using drugs:
    • Glucocorticoids - Suppress Ig production of B cells. Suppress IL genes (T cell proliferation). Prevent inflammation.
    • Cryostatics - Inhibit cell division (T and B cells).
    • Drugs acting on immunophilins - Block functions of immune cells
    • Using antibody treatments: target immune cells
    • Total body irradiation: Haemopoetic stem cell transplant. Lungs shielded. Removes residual cancer cells.
    • Blood transfusions
  52. What are the three classes of MHC molecules?
    • Membrane surface molecules (Class I & II): Involved in antigen presentation to T cells. Identify self and non-self cells
    • Diverse secreted factors/proteins (Class III): Not on cell membranes but expressed by cells: Complement, cytokines, enzymes, heat shock proteins and more…
  53. What is the function of MHCs?
    • Immune reactions and recognition of self:
    • Class I MHC - monitor self cells (healthy/unhealthy cells)
    • Class II MHC - recognition of foreign molecules
    • Bind antigens & present to T cells:
    • Class I to T cytotoxic cells (CD8)
    • Class II to T helper cells (CD4)
    • MHC combinations associated with different diseases & conditions E.g. Malaria:
    • Predict the likelihood of contracting certain disease
    • Breed animals for resistance to certain disease E.g. Scrapie (SCR: αA, A4, B6)
  54. What are the functions of complement?
    • Lyse cells/bacteria (Membrane Attack Complex)
    • Opsonize bacteria to enhance phagocytosis
    • Recruit (chemotaxis) and activate various cells: granulocytes and macrophages
    • Regulation of antibody response
    • Clearance of immune complexes and apoptotic cells
    • Detrimental effects for the host: Inflammation and tissue damage. Trigger anaphylaxis. Lack of leads to increased bacterial infections.
  55. What is the function of C3a (Anaphylatoxin)?
    • Can lead to anaphalyxsis due to:
    • Mast cell degranulation (histamine)
    • Smooth muscle contraction
    • Vasodilation: Dilation of the venules. Leukocyte extravasation.
    • Release of inflammatory cytokines. Increasing amount of acute phase proteins: anti-bacterial effects. TNFα: increase in body temperature or fever
    • C4a does the same but is weaker
  56. What is the function of C5a?
    • Chemotaxis: Attracts leukocytes (mostly neutrophils) to the site of invasion
    • Vasodilation: Allows for cells to cross venal membrane
  57. What is the function of C3b (opsonin)?
    • A recognition molecule for macrophages, granulocytes and cytotoxic lymphocytes
    • Coat surfaces of bacteria or immune complexes
    • Phagocytes have receptors for C3b - CR1 and CR3
    • Activate phagocytes for expression of receptors
    • Phagocytose coated pathogen/complex - Clearance from serum
  58. What is the function of C2a (Prokinin)?
    Cleaved by plasmin to yield kinin, which  results in edema
  59. What are the two types of pathogens?
    • Extracellular eg liver fluke
    • Intracellular eg malaria
  60. How does extracellular protection (antibody-mediated) occur?
    • Antibodies are the primary defence: Secreted IgG, IgA, IgE most common forms
    • They function in three major ways:
    • 1-Neutralisation of pathogen
    • 2-Opsonisation & ADCC (Antibody-Dependent Cell-mediated Cytotoxicity = killing)
    • 3-Complement activation
  61. How does neutralisation of toxins by antibodies occur?
    • 1) Formation of antibody-antigen complexes: bind free toxin;
    • 2) Prevents toxin binding to host cells and causing damage
    • 3) Antibody-antigen complexes are then engulfed by phagocytic cells (eg. Macrophage)(ie. a vacuum cleaner)
  62. How does opsinisation of bacteria by antibodie occur?
    • 1) Antibody acts as an opsonin: coats bacterial cell
    • 2) Encourages uptake of pathogen by phagocytic cell (e.g. macrophages, dendritic cell)
  63. How does complement activation by antibodies occur?
    • 1) Antibody bound to bacterial cell is then bound by C1qrs
    • 2) Classical complement pathway is activated
    • 3) Bacterial cell is lysed and ingested by Macrophages (ie. a vacuum cleaner)
  64. How does intracellular protection (t-cell mediated) occur?
    • Cell-mediated responses are the primary defence against intracellular pathogens
    • Approach is different depending upon where the pathogen resides in the host cell
    • In the cytosol: eg viruses and some bacteria. Killed by Cytotoxic T cells (known as Tc cells).
    • Within vesicles: eg some bacteria and parasites. Killed by action of helper T cells (known as Th1 cells).
  65. How does Tc cell killing of virus in the cytosol occur?
    • 1) Virus infects host cell- virus proteins are broken down by Proteasome in cell into peptides
    • 2) Peptides bind to MHC I which is then expressed on surface membrane
    • 3) Changed MHC I is detected by Tc cell (CD8+) so cell releases Cytokines (IL2, IFNγ, TNF) - infected cell is destroyed
  66. How does Th1 cell activation of infected macrophages occur?
    • 1) Macrophage infected by bacteria eg TB - resides in a vesicle
    • 2) Antigen peptides bind to MHC II. MHC II is expressed on surface membrane
    • 3) Th1 cell (CD4+) detects change in MHC II - activates infected macrophage to digest pathogen
  67. What is the process of B cell antigen presentation?
    • 1) antigen bound by BCR
    • 2) internalized to endosome
    • 3) processed to peptides
    • 4) peptide binds to MHC class II
    • 5) presented to T cells
  68. Which antigens do B cells recognise?
    • All must be in soluble form
    • Proteins: conformational determinants, peptide determinants exposed by proteolysis
    • Nucleic acids
    • Polysaccharides
    • Some lipids
    • Small chemicals (haptens)
  69. Which antigens do T cells recognise and how are they presented?
    • The majority of antigens are proteins. They are NOT in soluble form.
    • Fragmented to peptides, Bind to MHC I or II and are presented by MHC on the surface of nucleated cells.
    • T cells are grouped functionally
    • Th (CD4+): peptides associated with MHC II molecules
    • (recall: 4 by II = 8)
    • Tc (CD8+): peptides associated with MHC I molecules
    • (recall: 8 by I = 8)
  70. Why are there two different antigen processing pathways?
    • Each population of T cells recognises a particular type of antigen.
    • Viruses:
    • - peptide antigen associated with MHC I
    • - Tc kills infected cells
    • Bacteria:
    • - soluble peptide antigen associated with MHC II
    • - Th2 cells assist B cell to produce antibody & limit the growth
    • - intracellular bacteria grow inside vesicles
    • - Th1 cells activate macrophages to kill the intracellular bacteria
  71. What are the characteristics of dendritic cells?
    • Found in skin & other tissues
    • Ingest antigens, transport antigens to lymph nodes and spleen
    • The most effective APCs: present antigen to naive T cells
    • Present internalized antigens via MHC I or II
  72. What are the characterisitics of macrophages?
    • Ingest antigen by phagocytosis
    • Very good in activating memory T cells
    • Present peptides via Class II MHC
  73. What are the characteristics of B cells?
    • Bind antigen via surface Ig = BCR
    • Also ingest antigen by pinocytosis
    • Very good in activating memory T cells when the antigen concentration is low
    • Present peptides via Class II MHC
  74. What is cell mediated immunity?
    • Immunity facilitated by cells and hormones: T cells, NK cells and phagocytes (eg. macrophages, neutrophils). Secrete cytokines (= hormones).
    • Respond to intracellular pathogens (and cancer cells)
    • Immunity generated via T helper (Th) Cells: Secrete cytokines to activate T effector cells. e.g. IL-2 stimulates Tc cell proliferation & target cell lysis.
    • Not completely independent of humoral immunity
  75. Which cytokines are secreted by Th cells?
    • Th1 cells secrete IL-2, IFN-γ, IL12, TNF- α:
    • IL-2: stimulates Tc cell proliferation & cell lysis
    • IFN-γ: activates macrophages.
    • Th2 cells secrete IL-4, IL-5, IL-9, IL-10, IL-13:
    • Act as a helper for B cells
    • IL-4 & IL-5: drive B cell differentiation
  76. What causes Ig class switching to occur?
    Changes in the levels of various cytokines
  77. What is the 'balance' in immune responses?
    • Th1 is Pro-inflammatory: Tissue destructive, Virus defence, Intracellular bacteria, parasite defence.
    • Th2 is Anti-inflammatory: Allergy, Virus defence, Helminth defence, encapsulated bacteria defence.
  78. How does activation of the B cell occur?
    • 3 signals are needed
    • 1) recognition of antigen by BCR
    • 2) TCR recognises Peptide on MHC II
    • 3) Th cell releases cytokines to drive B cell division, differentiation and Ig class switching. IgG, IgE and IgA produced
  79. What is the characteristics of Tc cell-mediated killing of target cells?
    • Killing is antigen-specific
    • Killing requires cell contact
    • Tc cells are not injured when they lyse target cells
    • Each Tc cell is “multihit”- a “true assassin” - can kill numerous target cells; utilize several mechanisms to kill
    • These mechanisms include:
    • Perforins (protein that forms pore in target cell membrane)
    • Granzymes (damage cell; apoptosis = suicide)
    • Cytokines (TNF-α mediated killing = apoptosis = suicide)
  80. What are the killing mechanisms used by macrophages?
    • Secrete TNF-α (induces apoptosis = cell death)
    • Produce NO (damages cell proteins)
    • Produce superoxide, hydrogen peroxide (damage cell membranes)
    • Produce Cationic proteins and hydrolytic enzymes (damage membranes)
    • ADCC (Antibody Dependent Cellular Cytotoxicity
  81. What are the characteristics of activation of and killing by NK cells
  82. What do phagocytes (macrophages, neutrophils) release to kill cells?
    • Cationic proteins (to destroy cell walls)
    • Lysosomal acidic enzymes (to digest the carbohydrate of the cell walls of bacteria)
    • Oxyen radicals, peroxidases (are highly reactive; attack the cell wall; membranes)
  83. What is the relationship between F hepatica and bovine TB tests?
    • BTB diagnosis measures skin test response to TB antigen
    • Response measures Th1 cell response and IFN-γ
    • Fh suppresses Th1 responses
    • Fh compromises BTB diagnosis
  84. How can worms be used as therapy?
    • Apply worms to treat IBD and Crohn’s Disease in humans
    • Via Th2 response - Helminth antigens can suppress Th1 inflammatory response in the gut
  85. What is hypersensitivity?
    • Sensitisation to an antigen (Ag) by previous exposure - often repeated exposure over time
    • Re-exposure to Ag leads to an excessive response - Termed a “hypersensitivity” response which results in collateral damange as the immune system misdirects its response and attacks its own tissues.
  86. Give an example of each type of hypersensitivity reaction
    • Type I: (immediate - mucosal surface) Hayfever; Asthma; Eczema; flea allergy dermatitis in dogs
    • Type II: autoantibodies to red blood cells; Kidney damage
    • Type III: Farmer’s lung disease
    • Type IV: Skin contact reactions: TB, leprosy, parasites
  87. What is the process of type I hypersensitivity?
    • In the first exposure, IgE is produced, which binds to mast cells, basophils.
    • In the second exposure to the antigen, the IgE cross links causing mast cells to degranulate.
    • The release of Mediators eg histamine result in Local tissue Responses (vasodilation, oedema, bronchoconstriction, skin itching (pruritis)). This all happens rapidly (within 20 mins) so it is considered immediate. It is mast-cell mediated.
  88. What is the process of type II hypersensitivity?
    Type II is antibody mediated hypersensitivity. In the initiating mechanism, antigen is bound to host tissues. The IgG/IgM then binds to the antigen on the tissue's cells which recruits NK cells and macrophages or activates a complement cascade, which lyse the cell. This can cause severe damage, long term illness and possibly death. It takes 5-8 hours so is considered intermediate.
  89. What is the process of type III hypersensitivity?
    • Type III is immune-complex mediated. Immune-complexes bind to tissue as insoluble complexes or as a result of their increased size.
    • Once deposited, complexes bind complement and trigger CDCC, ADCC and inflammatory reactions as in Type II over a 4-10h period.
  90. What is the process of type IV hypersensitivity?
    • Type IV hypersensitivity is cell mediated.
    • During the sensitisation phase:
    • - Antigen is taken up by APC and presents it on its surface in MHC class II. This allows Th cells to recognise the antigen - this is the "first exposure"
    • - Memory Th1 cells specific for this antigen are generated
    • During re-exposure:
    • - Th1 memory cells re-encounter antigen and then become activated.
    • - This causes Th1 to secrete cytokines (IFN-y - activates macrophages) and chemokines (attract neutrophils, basophils etc.) to recruit pro-inflammatory cells and amplify inflammation.
    • - More T cells (CD4 and CD8) may also be recruited to the area
    • This reaction tends to happen in the skin - so when an inflammatory response occurs, redness, swelling and a bump may be present, which will represent the accumulation of T cells to the site. The reaction time is commonly 21-28 days.
  91. What is the role of Treg cells?
    • Mediate immune suppression by:
    • Inhibitory cytokines
    • Cytolysis
    • Metabolic disruption
    • Targeting dendritic cells
  92. What are the two types of regulatory T cells?
    • T regs and Tr1, which are both derived from CD4+ T cells.
    • Treg is termed “natural” as it is always active in the body. It suppresses via direct contact with Th1 or Th2 cells.
    • Tr1 cells are induced to release IL10 which suppresses Th1 responses. Tr1 recognise peptides via MHC
  93. What does the Hygeine hypothesis say?
    • Our modern “hygienic” lifestyle in childhood has led to rise in allergy and autoimmune disease. The modern 'hygienic' lifestyle due to our indoor lifestyle with smaller families, early childhood vaccinations, and less exposure to pathogens. Exposure to pathogens is needed to drive Treg expansion. Certain helminth antigens may 'set' the Treg clock.
    • The hygiene hypothesis also says that there is a reduced rate of allergy due to growing up on a farm, having pets in the household, and having diverse gut microbiota.
  94. What is self tolerance?
    The negative selection of self-reactive cells. Failure is known as an autoimmune response.
  95. What are the two types of autoimmune disease?
    • Systemic- the auto-immunity is directed against an antigen that is present at many different sites and can include involvement of several organs (e.g. rheumatoid arthritis)
    • Organ specific - Organ specific means the auto-immunity is directed against a component of one particular type of organ. (e.g. Type 1 diabetes, Multiple sclerosis)
  96. What is the difference between primary and secondary autoimmune disease?
    • Primary is due to genetic susceptibility. There is no trigger factor required.
    • Secondary requires a trigger factor.
  97. What are some options for treatment of autoimmune disease?
    • Anti-inflammatory drugs: NSAIDS, Corticosteroids
    • Immunosuppressant drugs: Methotrexate
    • Radiation
    • Plasmapheresis
    • Cell Blocking Reagents - antibodies: Anti-CD20 (Rituxan), Anti-CD3 (Teplizumab)
    • Cytokine Blocking Reagents: TNF (Humira, Enbrel)
  98. What are corticosteroids?
    Corticosteroids regulate the expression of many genes, with a net anti-inflammatory effect. First, they reduce the production of inflammatory mediators, including cytokines, prostaglandins, and nitric oxide. Second, they inhibit inflammatory cell migration to sites of inflammation by inhibiting the expression of adhesion molecules. Third, corticosteroids promote the death by apoptosis of leukocytes and lymphocytes. They are used in transplant chemotherapy.
  99. How was the vaccine for smallpox created?
    • Edward Jenner inoculated James Phipps, a 13-year-old boy, with the vaccinia virus obtained from a young woman named Sarah Nelmes who had been accidentally infected by a cow
    • James Phipps was then found to be “secure” (immune) to smallpox - unsuccessful challenge with variola virus “some months afterwards”.
  100. What is the difference between immunisation and vaccination?
    • Immunisation is the administration of an antigen to a live host with the purpose of inducing an immune response.
    • Vaccination is immunisation for veterinary or public health purposes.
  101. What are the aims of vaccination?
    • Sterile immunity- prevent infection
    • Prevent disease eg malaria vaccine: patient infected but not ill
    • Cure current infection (therapeutic)
    • Reduce pathology
    • Alter physiological state (e.g. to alter hormones levels and prevent boar taint)
  102. How does the body respond to a vaccination?
    • Priming 1st Dose: a foreign substance is recognised by the immune system leading to a primary IgG immune response. This may be inadequate and slow. Memory cells are produced.
    • Booster/ 2nd dose: a second, faster immune response as more IgG follows the booster dose. Memory cells from the primary response are triggered to produce IgG forming cells. It is known a prime-boost vaccine.
  103. What are the components of a vaccine?
    Infectious agent or specific antigen, adjuvant, stabilizers, preservative, buffers and salts.
  104. What are the characteristics of live attenuated vaccines?
    • Live bacteria or viruses are treated so they are no longer virulent - cannot cause severe disease.
    • The organism is modified so it mimics the virulent form - causes the body to mount an immune response
    • The organisms in the vaccine multiply in the recipient animal - gives better immunity than killed vaccines.
    • Used against bacteria, viruses (lung worm)
  105. What are the advantages and disadvantages of live vaccines?
    • Advantages:
    • Strong, long lasting immunity.
    • Fewer doses required.
    • Adjuvants not necessary.
    • Fewer adverse reactions.
    • Disadvantages:
    • May cause a mild form of the disease.
    • May cause abortion.
    • Limited shelf life.
    • Needs cold storage.
  106. What are the characteristics of killed/inactivated vaccines?
    • Killed infectious agents (eg using formalin) - still induce an immune response in the recipient.
    • Cannot cause disease and cannot replicate in the body - used for bacterial diseases and toxins.
  107. What are the advantages and disadvantages of killed/inactivated vaccines?
    • Advantages:
    • Rarely cause disease
    • Safe in pregnant animals and immuno-compromised animals
    • Usually have a long shelf life
    • Disadvantages:
    • Give only short lived immunity
    • Require multiple doses
    • Hypersensitivity reactions are common
    • Adjuvants can cause severe localised tissue reactions
  108. What are the characteristics of subunit vaccines?
    • It is not the whole organism that is used, only proteins - vaccines are safe, stable
    • Vaccines produced by genetic engineering - protein vaccines, DNA vaccines
  109. What are the advantages and disadvantages of subunit vaccines?
    • Advantages:
    • Theoretically cheap
    • Stable
    • Defined response
    • Less reactogenic
    • Combinations feasible
    • Disadvantages:
    • Narrow response
    • Multiple doses
    • Need for adjuvants
    • Organism can mutate away (lose efficacy)
    • Serotype selection
  110. What is an adjuvant?
    A substance which results in a specific increase in the immunogenicity of a vaccine component - it enhances immunity. E.g. liposomes, proteosomes, aluminium salts
  111. What is the cattle tick vaccine Bm86?
    A subunit antigen from tick gut. Vaccination induces IgG that damages tick’s gut - reduces egg production, transmission
  112. Describe the current vaccine status for Hydatid
    Hydatid vaccine EG95 is a subunit antigen from oncosphere. It shows high (>95%) efficacy, blocks invasion of oncosphere, and is now being tested in the field
  113. Describe the current vaccine status for Liver fluke
    • Liver fluke vaccines are subunit antigens from juvenile/adult flukes. Elicits <100% protection but may still induce production benefits
    • Blocks growth of juvenile flukes - flukes do not replicate in hosts
    • Threshold effects: <40 flukes, losses are minimal
    • Combination vaccines may be best approach: fluke vaccine is feasible- good news!
  114. Name the barriers of the Innate immune system
    • Epithelial barrier - made up of skin and mucous membranes
    • Physiological barrier - made up of different soluble components (e.g. temperature, low pH in stomach, chemical mediators)
    • Phagocytic barrier - Cells e.g. dendritic cells and macrogphages that can phagocytose. Cellular ingestion of pathogens/foreign particles.
    • Inflammatory barrier - redness, swelling, heat
  115. Name 3 chemical mediators
    Enzymes (lysozyme), peptides (alpha-defensins), complement, cytokindes (interferons, interleukins, TNF), acute phase proteins (haptoglobin, C-reactive protein), transferrin, lactoferrin
  116. Which belongs where?
    • Innate: Mucous membranes, mast cell, macrophage, lysozyme, skin, pH of stomach, natural killer cells (NK cells)
    • Adaptive: T cytotoxic (Tc) cells, T helper (Th) cells, Immunoglobulin, specific antibody, b cells, antigen presenting cells (APCs), adaptive
  117. What 3 cell types derive from haemopoietic stem cells?
    Lymphocytes (Lymphoid cells), granulocytes (myeloid cells) and red blood cells
  118. What does CD stand for?
    Cluster of differentiation
  119. What is the largest phagocytic cell?
    Macrophage
  120. Name the granulocytes
    Neutrophils, basophils, eosinophils, mast cells
  121. Where do all immune cells originate?
    Bone marrow
  122. Where are B cells found in aggregates in most lymphoid tissues?
    Germinal centres (in follicles)
  123. Secondary lymphoid organs/tissues are the site of what?
    Immune cell storage and antigen contact
  124. Name the two primary lymphoid organs where B cells and T cells mature in ruminants
    Ileal Peyer’s Patches and the Thymus
  125. Name the five classes of immunoglobulin
    IgM, IgG, IgD, IgE, IgA
  126. Which cells secrete antibody (immunoglobulin)?
    Plasma cells
  127. Ig is made up of … and … chains
    Two light and two heavy chains
  128. Name the specific antigen binding site on antibody
    Paratope
  129. Name the classes of immunoglobulin found in sheep
    IgG, IgM, IgE, IgA
  130. Which cells can switch antibody class?
    B cells
  131. Fab stands for what?
    Fragment antibody binding
  132. Name the specific site on antigen bound by antibody
    Epitope
  133. How many classes of Immunoglobulin are there in mice and which classes are they?
    IgM, IgG, IgE, IgD, IgA
  134. How do neonates and newborn mammals obtain antibody?
    Passive immunity – placenta or colostrum (depending on animal)
  135. Which part of the antigen is bound by antibody?
    Epitope
  136. What types of cells can be formed from an activated and differentiating B cell
    Plasma cells and memory B cells
  137. Which types of tissue grafting would be most successful: autograft, isograft, xenograft or allograft?
    Autograft (self) and isograft (genetically identical)
  138. MHC Class I molecules are found on the surface of which cells?
    All ‘self’ cells
  139. Which specific T cell and which specific CD molecule are involved in recognising MHC Class I?
    Class I: T cytotoxic – CD 8
  140. How do the MHC molecules differ in basic structure?
    • MHC Class I: Long alpha chain (3 domains), short beta chain (1 domain), 1 TM domain (alpha3 binds CD8)
    • MHC Class II: Same size alpha chain and beta chain (2 domains), 2 TM domains (beta2 binds CD4)
  141. What is the final product of all complement pathways?
    Membrane Attack Complex (MAC)
  142. Which pathway is activated by antibody (antibody dependent)?
    Classical pathway
  143. Which complement fragment acts as an opsonin?
    C3b
  144. What is the role of factor D in the Alternate pathway?
    Acts on Factor B -> fragments in Bb and Ba.
  145. What is the primary defence against extracellular threats (toxins, bacteria)?
    IgG
  146. How does IgG defend against toxins? How are toxins eliminated from the body?
    Neutralisation; cleared by macrophages
  147. What is the primary defence against intracellular threats (viruses, bacteria)?
    • T cells: what type?
    • Cytotoxic CD8+ T cells
  148. Which cells link the innate and adaptive immune response? Neutrophils? Macrophages? Eosinophils? Dendritic cells?
    Macrophages; dendritic cells
  149. What are the 3 key steps in immune recognition of antigens?
    • Processing of proteins to peptides
    • Binding of peptides to MHC I or II
    • Display of peptides to T cells via MHC
  150. What is a cytokine?
    Protein hormone that regulates the cellular response
  151. Name the two main types of T helper cells and key cytokines they produce
    • Th1 and Th2
    • Th1: IL-2, IFN-γ, IL12, TNF- α
    • Th2: IL-4, IL-5, IL-9, IL-10, IL-13
  152. What is the role of Th1 and Th2 cells?
    • Th1 cells are pro inflammatory
    • Th2 cells are anti inflammatory and pro antibody
  153. What are the 3 signals needed for a B cell response?
    • Binding of antigen by BCR
    • Presentation of peptide by MHC class II to T cell
    • Release of cytokine by Th cell
  154. Name 3 ways macrophages kill target cells
    • Cationic proteins
    • Nitric oxide= NO
    • Superoxide radicals
  155. What are the two types of autoimmune disease?
    Systemic or organ specific
  156. Name two ways regulatory T cell mediate immune responses
    Releasiing inhibitory cytokines, inducing cytolysis, causing metabolic disruption, targeting dendritic cells
  157. What are the 4 types of hypersensitivity reactions
    • Type I – immediate
    • Type II, III – Intermediate
    • Type IV – Delayed
  158. What are the 2 steps required for a hypersensitivity reaction?
    Immune sensitisation to antigen – prior exposure, and then re-exposure and clinical expression of the immune response
  159. What antibody and cells are involved in Type I reactions?
    IgE binding to Mast cells and basophils
  160. What antibody response determines the Type II reaction? What is the target antigen?
    IgG. Binding to cell surface/extracellular matrix antigens
  161. What antibody response determines the Type III reaction? What is the target antigen? How does it cause pathology?
    IgG. Soluble antigen. Complex deposition in tissues/blood vessels
  162. Which T cells are involved in theType IV hypersensititiy reaction? Given an example of an antigen that drives Type IV reponses.
    CD4 * Th1 and CD8 Cytotoxic Tx cells. Herbicides, insecticides, dyes and cosmetics; tuberculin (TB antigen)
  163. Name two types of regulatory T cells
    Treg is termed ‘natural’; always active in the body. Tr1 cells are induced by antigens
  164. What is the hygiene hypothesis?
    Our modern ‘hygienic’ lifestyle in childhood has led to a rise in allergy and autoimmune diseases
  165. Describe the physiological barrier of the innate immune response
    • Pathogen (bacteria, yeast, viruses) surpasses the epithelial barrier
    • Prevent establishment of pathogen growth by inducing fever (increased body temperature)
    • Normal body temp can prevent growth of some pathogens
    • The acidity of the stomach may also prevent pathogen growth.
    • Chemical mediators are:
    • -Soluble factors: Lysozyme in tears – enzyme
    • -Cell signalling: Cytokines – stimulate/attract (chemotaxis) immune cells
    • -Serum proteins: Complement, iron-binding proteins, c-reative proteins
  166. What are the five main types of antibody classes that can be produced in animals and which classes are produced in sheep?
    • 5 main classes:
    • Immunoglobulin M (IgM) - µ - pentameric
    • Immunoglobulin G (IgG) - γ
    • Immunoglobulin A (IgA) - α - dimeric
    • Immunoglobulin E (IgE) - ε
    • Immunoglobulin D (IgD) – δ
    • No IgD found in sheep, all others are.
  167. Name the 3 main types of cells that present antigen to T cells
    • Dendritic cells: Found in skin & other tissues. Ingest antigens, transport antigens to lymph nodes and spleen: T cell area. The most effective APCs: they present antigen to naive T cells. Present internalized antigens & MHC I or II.
    • Macrophage: Ingest antigen by phagocytosis. Very good in activating memory T cells.
    • B cells: Bind antigen via surface Ig and ingest antigen by pinocytosis. Very good in activating memory T cells when the antigen concentration is low.
  168. Name 3 ways phagocytes kill pathogens
    • Cationic proteins (which destroy cell walls)
    • Lysosomal acidic enzymes (to digest the carbohydrate of the cell walls of bacteria)
    • Oxygen radicals, peroxidases (are highly reactive; attack the cell wall; membranes)
  169. Name 3 reasons why we need veterinary vaccines
    • Improve health of domestic animals eg. pets (heartworm)
    • Improve animal production eg. sheep, cattle (gi nematodes, flukes, ticks)
    • Control zoonoses (threat to human health) eg. Liver flukes, dog hookworms, Toxoplasma
    • Reduce threat to export markets eg. Trichinella in crocodile meat
    • Control exotic disease threats eg. screw worm fly (Chrysomya), and surra (Trypanosoma) from SE Asia
  170. Name 3 main types of vaccines
    • Live vaccines - usually attenuated pathogen
    • Killed/ inactivated vaccines - killed (bacterial) or inactivated (virus or toxin)
    • Subunit - usually recombinant protein
  171. What is the primary defence against extracellular threats (toxins, bacteria)?
    IgG
  172. How does IgG defend against toxins? How are toxins eliminated from the body?
    Neutralisation of toxin; cleared by macrophages
  173. What is the primary defence against intracellular threats (viruses, bacteria)?
    Cytotoxic CD8+ T cells
  174. Which cells link the innate and adaptive immune response? Neutrophils? Macrophages? Eosinophils? Dendritic cells?
    Macrophages; dendritic cells
  175. What are the 3 key steps in immune recognition of antigens?
    • Processing of proteins to peptides
    • Binding of peptides to MHC I or II
    • Display of peptides to T cells via MHC

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