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Flashcards in Immunopathology Deck (39):

when are eosinophils involved in allergic responses



phases of hypersensitivity reactions

sensitisation phase effector phase immediate phase late phase: late effector phase


allergic response in airways leads to

decreased bronchial diameter and increased mucus --> nasal blockage, coughing, phlegm, asthma


what characterised an atopic patient?

- high levels of IgE - large numbers of eosinophils both in circulation and in tissues - large numbers of IL-4 secreting Th2 cells


very simply, the late effector phase of type 1 immediate hypersensitivity involves

eosinophilic activation and recruitment --> mediatorys --> epithelial cell activation, inflammatory cell recruitment and activation


how are allergens usually introduced to a patient

via a mucosal route


allergic response in skin leads to

increased fluid secretion and vasodilation --> swelling, itching and urticaria


very simply, the effector phase of type 1 immediate hypersensitivity involves

IgE binding to mast cells via FcR --> mast cell activation


what causes celiac disease

usually HLA DQ2 MHC molecule tTG2 in intestinal lamina propria normally deamidates gliadin peptides to change their glutamine side chain (positive) into glutamate (negative). This negative charge binds effectively to DQ2 on APC --> MALT --> Th1 activation --> cytokines - activate macrophages - damage to the villi


what is an allergy

an immune-mediated inflammatory response to common environmental antigens that are otherwise harmless


what molecules are in mast cell granules

histamine, heparin, tryptase +/- chymase, TNF-alpha


very simply, the sensitisation phase of type 1 immediate hypersensitivity involves

low dose allergen binds APC and basophils to activate Th2 and then initiate IgE


how do granulomas form in type 4 delayed hypersensitivity responses

macrophage activation by IFN-gamma results in the production of IL-8, IL-1 and TNF-alpha --> endothelial activation and phagocyte and lymphocyte migration --> TNF-alpha induce weight loss, granuloma formation and death of some infected macrophages


what is the allergen involved in celiac disease

gliadin component of gluten


timing of mast cell activation events

secretion of preformed mediators - 30-45 seconds synthesis and secretion of lipid mediators - 10-30 minutes synthesis and secretion of cytokines (slow)


what does the persistence of the antigen in the tissue result in

the accumulation of T cells and macrophages (via IFN-gamma) in the tissue releasing a lot of cytokines and ROS and RNS


what do eosinophils do in the allergic response

they produce: - toxic granule-derived basic proteins and free radicals --> tissue damage/remodelling. - chemical mediators --> epithelial activation, inflammatory cell recruitment and activation


what does celiac disease cause

damage to the vili of the small intestine


what is type 4 delayed hypersensitivity responses elicited by

a persistent antigenic stimulation (can be infectious agent or chemical agent)


what causes attraction and infiltration of eosinophils in allergic responses

chemokines by epithelial cells at inflammatory sites


where are mast cells located

mucosal and epithelial tissues, and near blood vessels


what is type 4 delayed hypersensitivity responses characterized by

cell mediated, heavy involvement of Th1 cells and macrophages, persistence of the antigen


allergic response in GI tract leads to

increased fluid secretion and peristalsis --> diarrhea and vomiting


what occurs in type 1 immediate hypersensitivity

an inflammatory response to allergens mediated by IgE


what causes eosinophil activation in allergic responses

IL-5 produced by Th2 and mast cells


what is the mechanism for type1 hypersensitivity

low dose allergen --> introduced via mucosal route --> DCs and basophils promote Th2 helper T cell activation via IL-4 --> TH2 cells produce IL-4, 5 and 13 --> promotes IgE secretion by B cells


how do dendritic cells and basophils activate Th2 cells in the sensitisation phase of type 1 hypersensitivity

DC binding to T cells produces IL-33 - which activate basophils --> produce IL-4 --> Th2 basophils can also be directly activated by allergen and binds T cells and produce IL-4 --> Th2


when mast cells are exposed to IgE initiated by the same allergen, what happens

IgE-FcR cross linking --> granule exocytosis (immediate effects) and synthesis of inflammatory lipid mediators (immediate effect, but slower than granules) and cytokines and chemokines (slower effect)


what are the 6 main contributors to Type 1 hypersensitivity

allergens Th2 cells IgE high affinity FcR Mast cells eosinophils


where are eosinophils normally located

in mucosal linings in very low numbers


allergic response in blood vessel leads to

increased blood flow and permeability of the blood vessels in the whole body --> increased tissue fluid and cell infiltrate --> anaphylatic shock


4 types of hypersensitivity

type 1 - immediate hypersensitivity type 2 - antibody mediated type 3 - immune complex type 4 - delayed type hypersensitivity


what are the phases of hypersensitivity

sensitization (very rapid) response (has immediate and late phases)


allergy treatment options

- adrenaline - anaphylaxis - inhaled beta-adrenergic receptor agonists - asthma - antihistamines (hives, allergic rhinitis) - corticosteroids


very simply, the late phase of type 1 immediate hypersensitivity involves

induced mediators causing cell infiltration and sustained oedema and/or SM contraction


how are mast cells sensitized

bind IgE (not bound to allergen) using high affinity FcR (very stable binding - can last for months/years)


what do the immediate phase and late phase of mast cell activation lead to

immediate - wheal and flare (localized swelling around site of challenge and BV dilation and engorgement) late - cell infiltration and sustained oedema and/or SM contraction


what does desensitization/immunotherapy involve

administration of increasing doses of allergen to achieve T cell tolerance -> switch to Th1 response


very simply, the immediate phase of type 1 immediate hypersensitivity involves

wheal and flare due to preformed mediators released by mast cells