front 1 what is hypersensitivity? | back 1 inappropriate secondary responses against harmless antigens result in more harm than benefit (the reaction is worse than the antigen) |
front 2 types of classification of hypersensitivity? | back 2 time until response mechanisms types of damage caused |
front 3 type I hypersensitivity mechanism | back 3 IgE |
front 4 type I hypersensitivity allergy | back 4 peanuts |
front 5 type II hypersensitivity mechanism | back 5 IgG/IgM (cells) |
front 6 type II hypersensitivity allergy | back 6 hemolytic anemia |
front 7 type II hypersensitivity transplantation | back 7 hyperacute rejection |
front 8 type II hypersensitivity autoimmunity | back 8 autoimmune hemolytic anemia |
front 9 type III hypersensitivity mechanism | back 9 IgG/IgM (IC) |
front 10 type III hypersensitivity allergy | back 10 serum sickness |
front 11 type III hypersensitivity transplantation | back 11 chronic rejection |
front 12 type III hypersensitivity autoimmunity | back 12 SLE |
front 13 type IV hypersensitivity mechanism | back 13 T cells |
front 14 type IV hypersensitivity allergy | back 14 poison ivy |
front 15 type IV hypersensitivity transplantation | back 15 acute rejection |
front 16 type IV hypersensitivity autoimmunity | back 16 type I diabetes |
front 17 which characteristics make parasites different than other pathogens? | back 17 they are multicellular organisms that are similar to humans they are too big for phagocytosis |
front 18 in general, what is the body's strategy to eliminate a parasite? | back 18 physical force for expulsion (coughing, sneezing, vomiting, diarrhea) increased mucus for protection |
front 19 what are the characteristics of type 2 immunity? | back 19 T(H)2 cells secrete cytokines that lead to IgE parasite specific IgE antibody binds to FceR on basophils, eosinophils, and most cells explosive reaction that dislodges that parasite from tissue that leads to expulsion attempts to minimize collateral damage |
front 20 example of type 2 immunity | back 20 IL-13 leads to mucous secretion; enterocyte turnover |
front 21 early phase isotype switching | back 21 complement fixation mast cell degranulation phagocytosis |
front 22 late phase isotype switching | back 22 immune complex formation |
front 23 IgG4 preferentially binds to | back 23 FcyRIIB which is inhibitory |
front 24 what are the unique structural/functional characteristics of IgE? | back 24 not soluble, but binds to FceRs IgE has asymmetric shrimp shape that binds with high affinity |
front 25 allergy associated with IgE | back 25 a type I hypersensitivity is an inappropriate IgE response against a harmless antigen most individuals will have response against these antigens but it's usually another antibody isotype |
front 26 two phases of hypersensitivity | back 26 the sensitization stage is the primary immune response to an antigen the effector stage is a secondary immune response to the same antigen |
front 27 what is omalizumab? | back 27 high affinity monoclonal antibody IgG specific for human IgE recognizes and binds the Fc region of the IgE; binds soluble IgE but not bound IgE prevents arming or sensitizing to the allergen does not lead to susceptibility to disease |
front 28 what are basophils? | back 28 basic-staining granulocytes: contain granules similar developmental program to eosinophils, but are then reciprocally regulated make up a very small percentage of leukocytes in the blood |
front 29 how do basophils help initiate TH2 response? | back 29 secrete TH2 polarizing cytokines (IL-4 and IL-13) express CD40L, which can bind to CD40 on B cells and drive isotype switching |
front 30 what are eosinophils? | back 30 granules are loaded with arginine-rich basic proteins named because they stain strongly with eosinophil like mast cells, external stimulus causes them to release toxins and inflammatory mediators reaction is highly toxic and damaging to host and parasite |
front 31 eosinophilia | back 31 abnormally high numbers of eosinophils damage to heart endocardium and to nerves |
front 32 what are mast cells? | back 32 present in all vascularized tissues maintain the integrity of the surrounding tissue alert immune system to trauma and infection repair damage caused by wounds and infection recruit neutrophils, eosinophils, and effector T cells, and growth factors |
front 33 what is the role of histamine in defense against parasites? | back 33 binds to one of four possible histamine receptors acute allergic reactions are often caused by histamine binding to H1 of smooth muscle and endothelial cells mast cells release TNFa which is complementary to histamine histamine release is immediate |
front 34 H1: | back 34 binding induces contraction of intestinal and bronchial smooth muscles, increased permeability of venules, and mucous secretion |
front 35 H2 | back 35 binding increases vasopermeability and vasodilation, stimulates exocrine glands, and increases stomach acid; also suppresses degranulation of mast cells/basophils in a negative feedback loop |
front 36 H3 | back 36 less involved in type 1: modulates neurotransmitter activity in CNS |
front 37 H4 | back 37 mediates mast cell chemotaxis |
front 38 secondary mediators | back 38 formed when membrane phospholipids are enzymatically cleaved into eicosanoids active at nanomle levels the overall function of mast cells degranulation is to circulating leukocytes. to the site of activation to amplify the reaction initiated by antigen cross-linking of IgE |
front 39 what is the purpose of tryptase, chymotryptase, and other proteases? | back 39 mast cells also make tryptase, chemotryptase, and other proteases; to help dislodge parasites |
front 40 molecular type of inhaled allergens that favor type 2 immunity and IgE production | back 40 proteins; they induce T-cell responses |
front 41 functions of inhaled allergens that favor type 2 immunity and IgE production | back 41 many allergens are proteases |
front 42 low dose of inhaled allergens that favor type 2 immunity and IgE production | back 42 favors activation of IL-4 producing TFH2 cells |
front 43 low molecular mass of inhaled allergens that favor type 2 immunity and IgE production | back 43 allows allergen to diffuse from particle to mucus |
front 44 high solubility of inhaled allergens that favor type 2 immunity and IgE production | back 44 allergen readily elutes from particle |
front 45 high stability of inhaled allergens that favor type 2 immunity and IgE production | back 45 allergen survives in desiccated particles |
front 46 peptides presented by MHC class II of inhaled allergens that favor type 2 immunity and IgE production | back 46 needed for T-cell activation |
front 47 what is sensitization? | back 47 the condition of a person who has been exposed once to an allergen and has made IgE antibodies against it |
front 48 common examples of sensitization | back 48 dried feces of the dust mite the specific antigen is a cysteine protease circulated currents from HVAC particles trapped in the mucous and carried to MHC II |
front 49 predisposing environmental factors of allergy | back 49 air pollution westernized countries low gut microbial diversity low fiber diet |
front 50 protective environmental factors of allergy | back 50 farm environment developing countries high gut microbial diversity high fiber diet |
front 51 MHC class II alteration | back 51 affects coding sequence enhanced presentation of allergen-derived peptides |
front 52 T-cell receptor alpha chain alteration | back 52 noncoding enhanced T-cell recognition of antigen-derived peptides |
front 53 TIM family alteration | back 53 promoter and coding sequence regulation of type 1/type 2 balance |
front 54 IL-4 alteration | back 54 promoter altered IL-4 expression |
front 55 IL-4 receptor alpha chain alterations | back 55 coding sequence increased signaling in response to IL-4 |
front 56 high-affinity IgE receptor beta chain alteration | back 56 coding sequence variation in the ligation of IgE by antigen |
front 57 5-lipoxygenase alteration | back 57 promoter variation in leukptriene production |
front 58 what are important cytokines involved in allergy? | back 58 IL-4,3,9,12,13, GM-CSF isotype switching, eosinophil survival, mast cell proliferation |
front 59 what is atopy | back 59 the tendency to develop abnormal TH2 responses to harmless antigens |
front 60 what are some examples of atopy? | back 60 allergic rhinitis asthma atopic dermatitis food allergies |
front 61 what is the wheel and flare? | back 61 a reaction observed when small amounts of allergen are injected into the dermis of an individual who is allergic to the antigen. it consists of a raised area of skin containing fluid (wheel) with a spreading, red, itchy reaction surrounding it (flare) |
front 62 what is the effector phase? | back 62 the effects of IgE-mediated allergic reaction will vary according to the site of cell activation |
front 63 early response | back 63 occurs within minutes of allergen exposure mediated by mast cell granule release of histamine, leukptrienes, and prostaglandins |
front 64 late response | back 64 occurs within hours later of allergen exposure a result of recruited cells cytokines released from mast cells increase expression of chemokines and CAMs on endothelium facilitating influx of neutrophils, eosinophils, and TH2 eosinophils play a large role in late-phase recruiting neutrophils and degranulation |
front 65 what are the symptoms of allergies in the blood? | back 65 increased vascular permeability; constriction of smooth muscle; blood pressure reduction; swelling (edema) in connective tissues leads to organ damage, impaired function, cause of death is often asphyxiation due to constriction of airway and swollen epiglottis |
front 66 anaphylaxis | back 66 release of IgE leads to mass activation of mast cells and basophils via IgE -> FceR interactions |
front 67 how is anaphylaxis treated? | back 67 stop exposure to the antigen manage ABC epinephrine injection trendelenburg position oxygen antihistamines corticosteroids epinephrine |
front 68 epinephrine | back 68 stimulates reformation of tight junctions in the vascular endothelium reduces permeability increased blood pressure relaxes bronchial smooth muscle stimulates the heart |
front 69 allergic rhinitis | back 69 hay fever allergens diffuse across mucous membrane and activate mucosal mast cells beneath it local edema causing obstruction of the nasal airways and nasal discharge |
front 70 allergic conjunctivitis | back 70 itchy, scratchy, watery eyes similar to allergic rhinitis, but at the eye |
front 71 allergic asthma | back 71 allergens activate submucosal mast cells in the lower airways of the respiratory tract leads to mast-cell degranulation and increased secretion of fluid and mucus into the respiratory tract bronchial constriction caused by contraction of smooth muscle chronic inflammation can lead to chronic asthma |
front 72 what are examples of allergies in the skin? | back 72 atopic dermatitis (eczema) atopic urticaria (hives) |
front 73 how do food allergies occur? | back 73 ingestion of antigen activates mucosal mast cells activated mast cells release histamine, which acts on epithelium, blood vessels, and smooth muscle antigen diffuses into blood vessels and is widely disseminated, causing urticaria |
front 74 how is type I sensitivity tested for? | back 74 skin testing is commonly used (it's cheap): injection of small quantities of known allergens under skin swelling and redness (resulting from local mast cell degranulation) indicate allergic response |
front 75 how is type I treatments tested for? | back 75 antihistamines bind and block H1 receptors on target cells leukotriene antagonists work in a manner similar to antihistamines inhalation corticosteroids inhibit innate immune cell activity in airways desensitization immunotherapy |
front 76 blood transfusions (type II hypersensitivity) | back 76 blood group antigens are carbohydrates people possess antibodies against the blood type they do not have if an individual receives a transfusion of the "wrong" type of blood, their antibodies will quickly attach to the donor blood cells and trigger complement proteins |
front 77 erythroblastosis fetalis (type II hypersensitivity) | back 77 hemolytic disease of the newborn; develops when maternal IgG antibodies specific to expressed RhD allele cross the placenta destroys fetal RBCs by binding and activating complement; causes child to be anemic as well as a build-up of toxic RBC |
front 78 hemolytic anemia (type II hypersensitivity) | back 78 can be drug induced some drugs can absorb nonspecifically to proteins on RBC membranes these drug-protein complexes may stimulate antibody production antibodies then bind to RBCs when the drug is present, stimulating complement mediated destruction penicillin can induce all four types of hypersensitivities under the correct circumstances for each other |
front 79 what mediates destruction in type III hypersensitivity? | back 79 immune complexes |
front 80 how does type III hypersensitivity occur? | back 80 if immune complexes aren't cleared effectively, they may deposit in tissues and can cause damage may trigger release of inflammatory mediators and vasoactive mediators proteases released may damage connective tissues clots may form as complexes activate platelets |
front 81 what are the symptoms of type III hypersenstivity? | back 81 fever, rashes, joint pain, lymph node, enlargement, and proteinuria vasculitis if in blood vessel autoantigens glomerulonephritis if in kidney arthritis in joints |
front 82 what is contact dermatitis? | back 82 sensitization can occur if a reactive chemical compound binds to skin proteins, which are modified and then presented to T cells could be induced by cosmetics, pharmaceuticals, industrial chemicals, metal ions, poison ivy, poison oak can cause strong cell mediated responses against skin cells, inducing blister like lesions and rashes |
front 83 what is chronic inflammation? | back 83 inflammation doesn't always resolve in a short period of time; it may last indefinitely, contributing to numerous other problems |