VETERINARY IMMUNOLOGY 380 FINAL EXAM QUESTIONS AND ANSWER

VETERINARY IMMUNOLOGY 380 FINAL EXAM QUESTIONS AND ANSWER Explain why blood typing and cross-matching are especially important before a blood transfusion in some exotic breeds of cats. - Answer-a. Breeds and Blood Types of Cats i. Domestic long and short hair cats - mostly type A ii. Exotic--Type B 1. Anti A natural- 1ml of type A blood into a type B cat will lead to shock and death iii. Type AB rare b. Before transfusing a cat, it is recommended to blood-type and cross-match Explain why it has been said that you can do one transfusion without a cross-match in the dog. - Answer-a. Upon first exposure there are NO NATURAL ANTIBODIES—with the second transfusion it would almost immediately cause a reaction b. No clinically significant natural antibody—1.1 and 1.2 though will cause issues on second transfusion if mismatched Explain the factors that result in hemolytic disease of the newborn. - Answer-a. Immune-mediated destruction of a neonate 's RBC by maternal antibodies i. Rh negative human mothers-- IgG (A and B are IgM and those cannot cross the placenta) --Ag induces IgG in mother--problem on subsequent pregnancies ii. A antigen in horses in immunogenic, so no natural antibody 1. Mare- no A Ag 2. Sire- A Ag 3. Foal- A Ag a. Not a problem in utero because no Ab can past through the placenta, if during partuition the mare is exposed to the A Ag twice Describe a major difference between the condition in humans and in foals. - Answer-a. Humans i. In utero in human because IgG does cross the placenta. (Rh factor) b. Foals i. After colostrum in foals Explain how Rhogam, in human medicine, prevents erythroblastosis fetalis in humans and how we prevent hemolytic disease of the newborn (HDN) in veterinary medicine. - Answer-a. Prevention of hemolytic disease of the fetus in humans is done by giving any Rh- mother RhoGam. i. RhoGam is passive antibody to the Rh factor. If the mother is exposed to the Rh antigen the passive antibody will prevent her from having an immune response to the Rh antigen. b. The passive antibody binds to the antigen and/or turns off B cells that would recognize the antigen (antibody feedback). For HDN in horses, explain what the best source for RBCs would be if a blood bank was not an option and what preparation (in general terms) would be required before giving the RBCs to the foal. - Answer-a. From the mother b. Mare doesn't have the A antigen (pic p4) Two dogs, Wrigley and Bush, are in for intradermal skin testing for allergies. Explain why Wrigley developed wheal and flare to ragweed and Bush did not and why they both developed wheal and flare to histamine. - Answer-a. Wrigley- ragweed injected and gets wheal (edema) and flare (red) because of IgE to Ragweed on mast cells causing crosslinking and degranulation (seconds-histamine to minutes-LTB4) (histamine causes vasodialation) i. Mimicking mast cell degranulation b. Bush- ragweed injection and no rxn because no IgE to ragweed i. Mimicking mast cell degranulation You explain to the owner that you will be blood-typing the cat and doing a major cross-match before giving the cat a transfusion. Please explain: a. Why do you do the major cross-match, i.e., what do you want to know? - Answer-i. Want to know does the recipient have antibody to the RBCs of the donor a. What do you mix together to do a major cross-match? - Answer-i. Donors—RBCs and Recipients—Plasma a. List two reactions of the cross-match that would indicate incompatibility? - Answer-i. Agglutination ii. Lysis of RBC because of complement a. You blood type the cat using the card test with antibody against the red cell antigen lyophilized on the card. There is agglutination under the B, and no agglutination under the A. What is the cat's blood type? Draw a picture of the cells and molecules leading to the result you see. - Answer-i. Blood type B (pic p5) a. If this cat is bred and the kittens have a different blood type than the queen, will the kittens have a problem in utero? Explain. - Answer-i. Not problem in utero because IgM doesn't cross the placenta in any species Describe the intradermal allergy test, including what is injected (general terms), what happens when an animal has an IgE-mediated allergy to what is injected, and why. - Answer-a. What is injected: potential allergen, to get Th2 you need a protein to initiate b. What happens in positive IgE mediated allergy: clinically you see the wheel and flare c. Why: because the histamine (increased vascular permeability and increased vasodilation) is released as well as mast cell degranulation--take 15-30 minutes (pic p5) Describe the clinical appearance of a positive and a negative result of the intradermal allergy test. Explain the mechanism of action that leads to the clinical response in the skin, including one or two molecules involved and their function. What would be used for a positive control in intradermal allergy testing? - Answer-a. Mechanism is degranulation of mast cells and release of histamine (seconds), leukotrienes (minutes), cytokines (hours) b. Immediate type hypersensitivity (15-20 minutes) c. Positive control?-- histamine Explain one mechanism involved in the success of allergen specific immunotherapy (ASIT). - Answer-a. ASIT is when the allergen is injected in low amounts and over time you add higher amounts to desensitize the animal b. Mechanisms: i. Induce Tregs TGFb secreted ii. IgA- will block the entry of the antigens Compare these therapies, including target and specificity: Apoquel (oclacitinib) Cytopoint (lokivetmab) Allergen-specific immunotherapy - Answer-a. Apoquel (oclacitinib) i. Target: signal transduction blocker- Jak STAT signaling to block IL31 but also block proinflammatory cytokines ii. Specificity: low specificity for IL31 b. Cytopoint (lokivetmab) i. Target: IL31 cytokine (acts on nerve endings causing itch) ii. Specificity: very specific for IL31 c. Allergen-specific immunotherapy i. Target: desensitization List the components of a Type III reaction and their role in the reaction - type of antibody, type of antigen, complement components (key molecules and their major function), neutrophils (why do they arrive, how are they activated, and what are the products of their activation), mast cells (how they are activated and the contribution of mediators). Review complement activation and mast cell degranulation if needed. - Answer-a. Antibody- IgG b. Antigen- Soluble c. Complement i. C3b opsonization for phagocytosis ii. C5a does chemotaxis of neutrophils (increase vascular permeability, activates neutrophils) iii. Anaphylatoxins-can happen because of C' fixation d. Neutrophils- C5a comes and granules have enzymes, defensin, antimicrobial peptides, O2 radicals, bleach, hydrogen peroxide e. Mast Cell- C5a and C3a, anaphylatoxins define anaphalaxis - Answer-a. Anaphylaxis: Rapid, generalized mast cell degranulation followed by eosinophil degranulation--leads to shock - smooth muscle contraction, increased vascular permeability define sensitization - Answer-a. Sensitization: An abnormal primary response to an antigen (sensitizing agent) such that, in a subsequent exposure, the individual mounts an excessive or abnormal secondary response that causes disease rather than immunity Explain the difference in a post-vaccination response of low-grade fever, lack of appetite, and lethargy the day after vaccination including timing and mechanism (important cells and molecules). - Answer-a. Post-vaccination response day after: 24 hours—Results in release of the pro-inflammatory cytokines (IL1, IL6, TNF) i. Seen on first dose—like puppies with first vaccination Explain the difference in a post-vaccination response of low-grade fever, lack of appetite, and lethargy in an immediate-type hypersensitivity reaction, including timing and mechanism (important cells and molecules). - Answer-a. Immediate-type hypersensitivity: ¼-1 hour--IgE (instead of preferred IgG) following a vaccination located on mast cells. On subsequent exposure to the antigen, IgE on the mast cells is cross-linked and the mast cell degranulates i. Need a period of sensitization so occurs after the dog previously been vaccinated (exposed to the antigen) ii. IgE-medicated hypersensitivity signs (mast cell degranulation due to IgE cross linking): 1. Local: a. Swelling of muzzle, ears and eyes b. Pruritus and rubbing face 2. Systemic a. Anaphylaxis b. Severe reactions include vomiting, diarrhea, and respiratory distress i. Give epinephrine for bronchodialation Describe how cellular targets are destroyed. Compare and contrast to other killing mechanisms discussed. - Answer-a. Complement fixation and cell lysis i. Classical pathway—so lysed via MAC (membrane attack complex) b. Opsonization for phagocytosis or agglutination i. Neutrophils and macrophages ii. Cause necrosis c. NK cell for ADCC i. Activate caspase cascade and apoptosis Define natural antibodies. - Answer-a. Natural antibodies = blood type--IgM isotype; the B cells do not isotype switch b. Thought to be formed as a result of normal flora of the gut, and there are cross-reacting epitopes with the RBC antigens Define blood-typing and cross-match and explain the tests used to determine each. - Answer-a. Blood typing--Looking for antigen on the red blood cell b. Cross matching—Major- does the recipient have Ab to the donor RBC that will destroy the RBCs Explain the purpose of blood typing and cross-matching and why they are important. - Answer-a. Blood typing-want to know what antigens are on the animals red blood cells --to determine if they will be destroyed or not Compare and contrast Type I and Type III hypersensitivity reactions - antibody, antigen, cellular infiltrate, and timing. - Answer-a. Type I—15-30 min i. Ab: IgE mediated ii. Ag: allergen, soluble iii. Infiltrate: eosinophils b. Type III—6-8 hrs later i. Ab: IgG mediated ii. Ag: soluble protein iii. Infiltrates: neutrophils Describe a classic example of a local immune-complex reaction, e.g., a booster vaccination. - Answer-a. Arthus reaction: local, normally from a booster dose because individuals have very high titered antibody in the circulation Describe a classic example of a systemic immune-complex disease, e.g., serum sickness, including the common sites of immune complex deposition, and explain the resulting clinical signs. - Answer-a. Serum sickness - a large amount of passive antibody administered - b. Common sites of deposition- joint fluid, skin lymphatics--plasma infiltrate c. Clinical signs- inflammation, arthritis, rash, nephritis Describe the series of events that occurs to result in a positive intradermal skin test for tuberculosis and what a positive intradermal skin test means. - Answer-a. A positive result on a TB skin test is a DTH (TB is intravesicular pathogen) b. Inject purified protein derivative (PPD TB) into dermis c. Sentinel cells pick it up (dendritic, mast cell, and macrophages) lead to proinflammatory cytokines and act on endothelial cells to upregulate addressin molecules of the blood vessels d. Taken up and processed and presented exogenously on MHCII (sentinel cells are professional presenters) e. The memory lymphocytes and neutrophils are exiting at the site of inflammation to see if they are needed f. Immune response to intravesicular is Th1 which secretes IFNy g. In 3 days the vet goes and palpates the induration (feels like a pea), the neutrophil and immediate response molecules have left Explain the difference between a positive intradermal skin test for determining allergen selection for a dog with atopy and a positive intradermal skin test for a cow infected with Mycobacterium bovis, including the antigen specific component of the immune system, the clinical presentation, the cause of the reaction, and the timing of the observable reaction. - Answer-Intradermal allergen Ag specific component--IgE Clinical sign--wheal and flare Causes Rxn--mast cell degranulation, histamine Timing--15 min Intradermal TB Ag specific component--Th1 Clinical sign--Induration Causes Rxn--TH1 cytokines w/ IFNy and mononuclear cell accumulation Timing--72 hr There is a product on the market called VenomVet™ for the treatment of people for all North American pit viper envenomations. Use labeled drawings and brief notes to describe how the antivenin was treated to make this product. Give a brief explanation for why it will still work as an antivenin and decrease the risk of developing serum sickness. Do you think this would also work to treat envenimation in animals? Why, or why not? - Answer-a. Serum sickness is ab to ab (antivenom is an ab) b. Venom binds to its antivenom receptor which neutralizes it c. Without the Fc there is no complement fixation because you cant bind and decreases inflammation, and decreased phagocytosis, decrease size and epitopes d. Oils and lipids are not good antigens because there is no protein, so no T cell help (only foreign) e. IgM or IgG mediated f. This is both exogenous and endogenous g. Positive correlation between the amount of antivenom administered and clinical signs h. VenomVet -equine IgG cleaved at the hinge, Fab2 (pic p8) Do you thin urushiol oil alone would be a good antigen? Explain. - Answer-o No because it is not large or a protein; it is only foreign What is the general term used to describe this type of new antigen (immunogen)? - Answer-o Hapten carrier • Based on the description of this immunogen, describe how it would be processed and presented to the immune system, including the antigen-specific cells stimulated. - Answer---extracellular (CD4)(exogenous MHC2) --intracellularly (CD8)(endogenously MHC1) List two general categories of tumor antigens - Answer---overexpress self antigens --mutations Describe the important innate and adaptive cellular immune response to tumor cells, how they recognize the tumor cell and how they contribute to tumor cell death. - Answer-Innate: i. Recognize: NK cells activated by IL12—kill cells not expressing normal MHCI, ADCC, or expressing stress proteins (MICA/MICB) ii. Tumor death: Apoptosis Adaptive i. Recognize: T cells- CD4 and CD8—kill cells with peptide on MHCI ii. Tumor death: Apoptosis (perforin granzyme, caspase cascade), Antibodies (from Th1) cause opsonin for phagocytosis, macrophages (become M1 from Th1), neutrophils (lysosomal enzymes, bleach, HCl) List three ways tumor cells evade being detected by the immune system. - Answer--low expression of MHCI -tolerance -secrete TGFb to suppress immune system Describe one type of immunotherapy used to treat cancer (other than vaccine). Pick one and learn all about it - Answer-Chimeric Antigen Receptors -recombinant receptors for specific tumor Ag -is chimerized with a special signaling tail -transfected into T cells -receptor binds to tumor Ag it signals the killing mechanism of the T cell Explain how the canine melanoma vaccine works - including the type of tumor antigen targeted, the type of vaccine, and how it works to destroy the tumor. - Answer-Type of tumor antigen targeted: tyrosinase which is overexpressed on Melanoma cells Type of vaccine: nucleic acid--DNA vaccine with gene for human tyrosinase inserted into a DNA plasmid Immune response: i. Intracellular- CTL ii. Extracellular- activates Th1, Th2 iii. B cells see it and reacts with help to class switch and become a plasma cell to make IgG iv. Human tyrosinase is different enough but will still trigger the dog immune system—cross reactions How it works: i. ADCC 1. NK cells--apoptosis 2. Macrophages 3. Neutrophils ii. Th1 1. Cytokines like IFNy iii. CTL apoptosis 1. List two risks and two benefits of vaccines. - Answer-a. Risks i. Hypersensitivities (anaphalaxis) ii. Localized reactions iii. Non-specific systemic side effects (proinflammatory cytokines) b. Benefits i. Control of zoonotic diseases, e.g. rabies ii. Reduction of animal suffering Define core and non-core vaccines. - Answer-a. Core vaccines i. Recommended for all healthy animals b. Non-core vaccines i. Recommended based on risk of exposure Recommended depending on geographic region, patient lifestyle, age, etc 1. Describe the basic immunology for a protective adaptive immune response to: a. Extracellular pathogen (bacterial) - Answer-i. Stimulate IgG—Th1, Th17—neutrophils ii. MHCII presentation --opsonize for phagocytosis 1. Describe the basic immunology for a protective adaptive immune response to: a. Intravesicular pathogen (vesicle bound) - Answer-i. Stimulate Th1 with IFNy for M1 macrophages ii. MHCII presentation --kill organism inside cell 1. Describe the basic immunology for a protective adaptive immune response to: a. Intracellular pathogen (viral) - Answer-i. Want CTLs ii. Th1 cytokines and IFNy to get IgG iii. MHCI and MHCII presentation --want to neutralize the virus 1. Describe the basic immunology for a protective adaptive immune response to: a. Mucosal pathogen - Answer-i. Mucosal antibody (sIgA) or for parasite would want IgE ii. Intranasal/oral vaccine necessary 1. When given the characteristics and pathogenesis of a disease, describe the type of immunity you would like an ideal vaccine to induce. - Answer-a. Say Influenza? —MLV intranasal or oral vaccine to get to mucosal surfaces and get IgG i. mucosal ab, neutralizing ab, cytotoxic t cells, IFNs, Th1, gamma delta t cells b. Newborn calf- likely just getting neutralizing ab from IgG c. Bacteria—likely induce ab against the external characteristics d. Viral—cellular response is needed 1. List three governmental agencies involved in regulating veterinary products and give examples of the products they regulate. Explain the difference between biologics and pharmaceuticals. - Answer-a. Food and drug administration (FDA)—pharmaceuticals- antibiotics b. Environmental Protection Agency (EPA): Topical insecticides c. United States Department of Agriculture (USDA) - Center for Veterinary Biologics (CVB) - regulates veterinary biologics i. Biologics—vaccines List the basic characteristics/qualities of all USDA fully-licensed vaccines, i.e., what they are and what they are not - Answer-a. Pure, safe, potent, and efficacious b. NOT worthless, contaminated, dangerous, or harmful List the differences in assurances for safety and efficacy for a fully licensed vaccine - Answer-a. Fully licensed- efficacious and safe List the differences in assurances for safety and efficacy for a conditional vaccine - Answer-b. Conditional license- to meet an emergency situation or other special circumstance i. An expedited procedure which assures safety and a reasonable expectation of efficacy List the differences in assurances for safety and efficacy for an autogenous vaccine - Answer-c. Autogenous- limited safety and no efficacy testing i. Always killed ii. Produced in a USDA licensed facility iii. Some safety and sterility testing required List the differences in assurances for safety and efficacy for a intentional vaccine - Answer-d. Intention- Allows the control of time of disease introduction (feedback) i. Serious safety problems (no safety testing and no efficacy) ii. May be more virulent than anticipated Describe information on a vaccine label for a recently licensed vaccine - Answer-1. For the vaccination of healthy (animal) against the (system) form of disease caused by (microorganism). 2. Minimum age, schedule, dose, and revaccination recommendations also to be included on the label. 3. Further information available on a public website: study design, challenge data, efficacy study outcome/results List one-two advantages and disadvantages of each MLV vaccines and killed vaccines and bacterins. - Answer-a. MLV i. Advantages—more rapid protection (CTL, Th, and Ab because presented both endogenously and exogenously), 1 dose required ii. Disadvantages—abortion, immunosuppressive b. Killed i. Advantages—safer, no reversion to virulence ii. Disadvantages—increased risk of hypersensitivity (type 1), no CTL Give an example of a new technology vaccine and how it differs from traditional killed and MLV vaccines. - Answer-a. mRNA vaccines i. giving nucleic acid---like Covid vaccine -animal makes the protein so it is more pure and specific Explain what DIVA means in the veterinary vaccine world and the advantages of using DIVA vaccines. - Answer-a. Detecting Infection in Vaccinated Animals b. Allows you to detect infection in a vaccinated animal c. Important for control and eradication of disease; allow for vaccination while retaining ability for serologic surveillance for infection --ab from maternal or infection or vaccination or previous infection Describe the role of adjuvants in vaccines and give an example. - Answer-a. Added to vaccines to enhance immunity by triggering danger signals (PAMPS and DAMPS) in innate system b. Examples: chemicals, microbial components Explain the various factors that can be reasons a vaccine fails to protect. - Answer-a. Problem with vaccine handling—storage temperature or exposure to light b. Administration—wrong route, partial dose c. Vaccine strain differs from field strain—problem with RNA viruses 1. When given a scenario, provide an explanation for why a vaccine might fail or induce an insufficient response. - Answer-a. Immunodeficiency b. Age c. Poor health/nutrition d. Toxins e. Infectious disease f. Stress g. Concurrent infection List and explain three mechanisms of how maternal antibody can interfere with vaccination - Answer-a. Negative feedback by IgG on Ab production i. Turns B cell off b. Neutralize MLV i. Depends on efficiency of neutralization c. Increased removal of killed antigen List at least two factors that influence the response to vaccination in the presence of maternal antibody - Answer-a. Maternal antibody titer b. Type of vaccine c. Type of pathogen Define window of susceptibility. - Answer-a. Time between when the virulent virus can breakthrough and the MLV can stimulate antibody production in the newborn to a protective level. This is when the newborn is most vulnerable Explain what it means to "breakthrough" maternal antibody when talking about susceptibility to disease and vaccination in young animals and the associated challenges. - Answer-minimum maternal antibody titer that a modified live vaccine virus can "breakthrough" and stimulate the neonate's immune response. This is a lower titer than the titer a virulent virus can "breakthrough." Describe at least three factors that influence the duration of immunity for a vaccine and describe how duration of immunity is determined for vaccines. - Answer-a. Type of vaccine b. Type of disease c. Animal itself d. Duration of immunity is determined through epidemiology studies When given clinical signs that develop in an animal post-vaccination, provide a reasonable explanation for the mechanistic basis for that adverse vaccine reaction. - Answer----Problem with vaccine or administration i. Virulence of MLV in alternate species ii. Extraneous agent iii. Residual virulence on MLV ---Adverse vaccine reaction due to excessive induction of cytokine release ---hypersensitivity i. Type 1—anaphalaxis-IgE ii. Type 2—erythrocyte antigens iii. Type 3—arthus rxn at injection site b. 24 hrs after vaccine—general sick feeling—proinflammatory cytokines acting on liver and APP c. 15-30min after vaccine—on booster dose-swollen lips, itchy eyes—mast cell degranulation from IgE crosslinking. Histamine, leukotrienes all acting on nerve endings making itchy Based on the Moore studies, explain what factors are associated with increased adverse vaccine events in dogs. - Answer-a. Small dogs- more likely to have adverse rxn—so weight b. Number of vaccines gives per office visit (not antigens cause there are lots of antigens in each vaccine) Explain how an animal may have immunity to a pathogen, but not have detectable circulating antibody. - Answer-no circulating antibody but T cell mediated immunity and sIgA List two to three factors that can optimize vaccine efficacy and duration of immunity and minimize adverse reactions. - Answer-a. Only use vaccines that are indicated for the patient's situation b. Vaccinate animals at high risk of exposure more often Compare and contrast primary and secondary immunodeficiency. - Answer-Primary i. Rare, inherited or developmental ii. Generally not reversible iii. Examples: BLAD, SCID Secondary i. Very common, acquired ii. Generally reversable iii. Examples: infectious agents, noninfectious disease, drugs/therapies, toxic compounds, physiologic conditions Describe two clinical manifestations that would suggest immunosuppression may be contributing to the problem. - Answer--Infection with opportunistic organisms -Reccurent and/or chronic protracted course of infection Illustrate and explain with a labeled drawing how it is often the additive effect of immunosuppressive factors that result in clinical disease and not one factor alone. Label the Y-axis and include at least two factors that decrease resistance to disease and one factor that will boost or increase resistance. - Answer-pic p14 List the four types of hypersensitivity and the basic mechanism of each. - Answer-i. Hypersensitivity is antigen specific so it is adaptive immunity b. Type 1: Immediate; mediated by IgE, mast cells degranulation you immediately see clinical signs, eosinophils; examples are anaphylaxis, atopy c. Type 2: Cytotoxic type, mediated by Ab (IgG or IgM) and complement/phagocytosis; an example is blood transfusion reactions, many autoimmune diseases d. Type 3: Immune-complex type; mediated by accumulation of immune-complexes (IgG or soluble ag) and response to them; an example is serum sickness e. Type 4: T-cell-mediated (delayed-type)- two types - 1) soluble antigen and mediated by TH1 activation of macrophage; an example is TB positive skin test; 2) cell-associated antigens mediated by CTLs; an example is contact dermatitis. Define sensitization. - Answer-a. An abnormal primary response to an antigen (sensitizing agent) such that, in a subsequent exposure, the individual mounts an excessive or abnormal secondary response that causes disease rather than immunity Explain the important factors responsible for IgE production, e.g., type of antigen, location in the body, antigen-presenting cell, TH cells, B cell, cytokines. - Answer-a. IgE production--good for helmithic parasites i. Type of antigen: allergens ii. Location in body: all different ways iii. Antigen-presenting cell: on MHCII, tells naïve T helper 0 to become Th2 (by IL4) iv. T Helper cell: T Helper 2 v. B cell: undergoes class switching from the cytokines to make IgE vi. Cytokines: IL4, IL5, IL10, IL13 List the cell responsible for the early phase immediate-type hypersensitivity reaction and special features of that cell (e.g., Fcε receptors). - Answer-a. MAST CELL-- degranulation- clinical signs are due to the mediators released from the mast cell b. If enough antigen it will crosslink to the Fab (see picture p1) List the three waves of mediators released from mast cells during IgE mediated degranulation, approximately when they are released, and give an example of a mediator from each wave, including function. (seconds) - Answer-a. Seconds - immediate release - preformed and stored in granules i. Toxic mediators - e.g., histamine, heparin, serotonin 1. Toxic to parasites ii. Function—increase vascular permeability, increase vasodilation, bronchoconstriction List the three waves of mediators released from mast cells during IgE mediated degranulation, approximately when they are released, and give an example of a mediator from each wave, including function. (minutes) - Answer-b. Minutes following activation, products from membrane phospholipids are generated i. Leukotrienes (SAME AS HISTAMINE), PAF are very potent molecules, more potent than histamine. They cause: 1. Smooth muscle contraction (bronchoconstriction) 2. Increased vascular permeability List the three waves of mediators released from mast cells during IgE mediated degranulation, approximately when they are released, and give an example of a mediator from each wave, including function. (hours) - Answer-c. Hours following activation i. Cytokines are synthesized. e.g., IL4, IL5, IL13 1. IL4, IL13 - stimulate and result in the production of more TH2 - this adds to the allergy cycle- the more TH2, the more IgE from B cells, and the more mast cells sensitized to degranulate. 2. IL5 - promote eosinophil production and activation Define hypersensitivity - Answer-a. Hypersensitivity: These are all memory responses--adaptive immune response directed toward innocuous substances such as self or pollen that induce damage to the host. An immunologically mediated damaging inflammatory response to a normally innocuous antigen. Define Allergy - Answer-a. Allergy: Something triggers the immune system to respond to foods and produce either TH2 and IgE or TH1 response and decreased Tregs Define atopy - Answer-a. Atopy: used for meaning a genetic predisposition