Chapter 19 and 20 Learning Objectives Define the following terms: Atopy Allergen Allergy Sensitization Elicitation Vasoactive amines Lipid mediators Mast cells Basophils Eosinophils Degranulation Vasodilation Bronchoconstriction Wheal and flare Urticaria Anaphylaxis Anaphylactic shock Autoreactive T cells Cross-reactivity Vasculitis Arthritis Nephritis Serum sickness Immunization DTH Neoantigen Granuloma Fibrosis Multinucleate giant cell Hypersensitivity Autoimmunity Histamine Antihistamine Prostaglandin Leukotriene Corticosteroids (Ant)agonist Learning Objectives – important concepts to know At the end of these chapters, you should be able to: 1. Discuss what a hypersensitivity response is. 2. List the three types of antigens that can elicit a hypersensitivity response. 3. Identify each of the hypersensitivity responses, including: a. the classification/type (by number and by name) b. what initiates the hypersensitivity response (ie. an antibody binding to an antigen on a cell/tissue) c. the mechanism(s) of action (also called the pathogenesis) that causes/results in tissue damage, including any subsequent local or systemic effects d. the cells and molecules involved in each hypersensitivity response e. examples of clinical diseases associated with each of the hypersensitivity responses f. available treatments for each of the hypersensitivity diseases discussed in lecture (specific treatments if mentioned in lecture) 4. Using examples, explain what allergens are. You may wish to use your text to identify the various types of allergens. 5. Identify what cytokine(s) is(are) best associated with the allergic response. 6. Discuss what is meant by when we say an individual is atopic. 7. Using Table 20-1 and your lecture notes, compare the three cell types that can participate in type I hypersensitivity responses including: a. their location in the body b. their granular contents (including their functions) c. their life span 8. Discuss the process by which mast cells are activated.9. List the 3 phases that occur once a mast cell has been activated, including naming the chemical mediators that are produced in each of these phases. Identify the rationale for the timeline in which they are released from the mast cell. What effects to each of these products have on the various sites within the body? Please be sure to list specific examples. 10. components make up this receptor and what functions do they provide? What does this receptor bind? 11. Identify the major signaling cascades and intracellular events that occur once an allergen activates a mast cell (the three phases). 12. Which of the numerous molecules released from the mast cell is (are) the most potent? 13. Discuss the purpose(s) of eosinophils. How are they recruited and subsequently activated? What molecules do they contain to assist them in performing their effector function? 14. Discuss the events that occur during the immediate and late-phase reaction of type I hypersensitivities. Be sure to also include the timeline of events in your discussion. 15. Explain the wheal and flare reaction. Identify examples of when this presentation would be observable and when we could induce this type of response. 16. Explain the hygiene hypothesis. What evidence exists to support this hypothesis? 17. Discuss anaphylaxis and anaphylactic shock. What are the most common inducers of this response? How can it be treated? How are these two reactions the same and how are they different? 18. Discuss the symptoms experienced by an individual with asthma and explain the underlying immunologic basis of these symptoms. What treatments are available for asthma patients and how do they work? 19. Describe the mechanism believed to be behind how allergy shots are used to treat and prevent type I hypersensitivities (desensitizing an individual against a particular allergen). 20. Briefly discuss other examples of allergens that can lead to an allergic response such as allergic rhinitis, food allergies, and urticaria. For each, discuss the classification of hypersensitivity response, the initiating event, and the effect on the body. 21. Explain how IgG can be an agonistic antibody and an antagonistic antibody at the same time. What are the two conditions associated with these scenarios? 22. Discuss the rational of how rheumatic fever contributes to type II and type III hypersensitivities. 23. Describe the sequence of events that occur during serum sickness.24. Discuss the structure and formation of a granuloma. Please note: For Table 19-2, you are responsible for the following diseases: a. autoimmune hemolytic anemia b. autoimmune thrombocytopenic purpura c. rheumatic fever d. myasthenia gravis e. Graves’ disease f. insulin-resistant diabetes For Table 19-3, you are responsible for the following diseases: a. systemic lupus erythematosus (SLE) (p. 411-412) b. post-streptococcal glomerulonephritis c. serum sickness For Table 19-4, you are responsible for all of the diseases listed in the table. - Rheumatoid arthritis (RA; p.412-413) - Multiple Sclerosis (MS; p.413-414) - type I diabetes (p.414-415) - inflammatory bowel disease (p.415) Please look up the following information in your textbook: In Table 20-2, you should be able to identify: - the chemical mediator/molecule along with the cell it is found in (you are responsible for knowing the following molecules: histamine, prostaglandin, leukotriene, IL-4, IL-5, various non-specific enzymes, TNF, major basic protein, and eosinophil cationic protein) - the effect (local or systemic) of each of the chemical mediators Please read the section on “Immunotherapy for Allergic Diseases” on p.