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WEEK 16:
Immune attack on tissues - hypersensitivity and allergy:
| Question | Answer |
|---|---|
| examples of antigen in type I hypersensitivity reaction (TI HSR) | dust, food (eg peanuts), animal dander, and insect envenomations (eg bees, wasps) |
| TH I or TH II is dependent on what | environment during development from immature CD4+ lymphocyte |
| activated TH2 lymphocytes produce what | interleukins 4, 13, and 5 |
| what are IL-4/5/13 responsible for (3) | making IgE from B cells, eosinophil activation, and mucus production |
| TH2 cells promote what | type I hypersensitivity |
| how does IL-4 made from TH2 work | IL-4 induces naive CD4+ T cells to become TH2 cells which make more IL-4 (and 5). IL-4 activates B cells to make IgE which bind to mast cells in first exposure. In second exposure, antigen binds to IgE, causing degranulation of mast cell. |
| how does IL-5 made from TH2 work | stimulate production and activation of eosinophils, helping them 'live' longer |
| mast cells/ basophils | both are granulocytes containing granules with histamine and heparin, which both bind Fc portion of IgE (tail) causing degranulation |
| what happens when histamine is released via degranulation of mast cells | increase vascular permeability so smooth muscle contracts in lung and blood vessels dilate |
| what happens when cytokines are released via degranulation of mast cells | cytokines IL4 and 13 are released which promote TH2 differentiation and promote IgE production. TNF alpha promotes tissue inflammation |
| what does IL-4 and IL-13 do | cytokines which promote TH2 differentiation and promote IgE production |
| what does TNF alpha do | promotes tissue inflammation |
| what happens when lipid mediators are released via degranulation of mast cells | lipid mediators eg leukotrienes and prostaglandins (PGD2) are released which increase vascular permeability and cause smooth muscle contraction |
| example of lipid mediators | leukotrienes and prostaglandins (PGD2) |
| TI HSR symptoms (8) | rhinitis, conjunctivitis, asthma, dermatitis, hives, vomiting, diarrhoea, systemic anaphylaxis |
| describe drug hypersensitivity in penicillin | metabolic intermediate causes reaction rather than whole intact drug |
| rhinitis | stuffy nose |
| conjunctivitis | itchy eyes |
| dermatitis | eczema |
| hives | urticaria |
| stridor | high pitched noise when breathing |
| what is laryngeal oedema associated with (3) | bee envenomation, penicillin, and peanuts |
| sequence of events in TI HSR | APC present allergens which activate T cells. Activated TH2 release IL-4 which induces naive CD4+ T cells to become TH2 cells that make more IL-4 and IL-5 |
| eosinophils nucleus | 2 lobes |
| eosinophil staining | granules in cytoplasm stain red |
| where are eosinophils found usually | parasitic infection sites |
| production of eosinophils is by what (2) | IL-5 and granulocyte-monocyte colony stimulating factor (GM-CSF) |
| life of eosinophils | live for several days in tissue |
| what happens to eosinophils when they are no longer stimulated by IL-5 | die via apoptosis |
| anaphylaxis | rapid onset allergic reaction which can cause death caused by an acute generalised IgE mediated immune reaction involving specific antigen, mast cells and basophils |
| symptoms of anaphylaxis | widespread urticaria, cardiovascular collapse, laryngeal oedema, airway obstruction and respiratory arrest |
| skin prick test | most effective test to detect IgE mediated type I allergic reactions |
| what should you see in a TI HSR using a skin prick test | wheal and flare from common environmental antigens |
| results of the skin test reactivity depend on what (3) | intact immune system, presence of IgE sensitised mast cells that release mediators when exposed, if the patient takes anti-histamines and other medications 48 hours before the test |
| wheal | raised bump |
| flare | redness around bump |
| atopy | individuals producing a large amount of IgE antigen after exposure to everyday antigens eg asthma, hay fever, eczema |
| early phase responses to TI HSR | fast response due to mast cell degranulation, and responsive to antihistamines |
| late phase responses (LPR) to TI HSR | mediated by TH2 cells recognising epitopes, and recruit eosinophils. Do not respond to antihistamines and requires immune modulators eg corticosteroids |
| TII HSR | second exposure where an antibody (IgG/ IgM) is directed against antigens on cell membrane/ in ECM |
| how does IgM mediated TII HSR work | lysis via membrane attack complex (C5-C9) |
| lysis | destroy cell by breaking cell membrane/cell wall |
| example of TII HSR mediated by IgG | haemolytic anaemia in newborn |
| how does IgG mediated TII HSR work | IgG attaches to basement membrane/ matrix and activates complement system |
| examples of IgG mediated TII HSR | goodpasture syndrome and pernicious anaemia |
| pernicious anemia | inability to absorb vitamin B12 because IgG is directed against proton pump in parietal cells |
| goodpasture syndrome | IgG against pulmonary and glomerular capillary basement membranes |
| haemolytic anaemia in newborn | group O blood from other (has anti-A/B/IgG) crosses placenta and attach to fetal blood (group A/B without the same anitbodies). Fetal blood is phagocytosed by splenic macrophages |
| TIII HSR | immune complexes eg IgG deposited in tissue activate complement system and produce C5a which attract neutrophils to further damage tissue |
| what usually happens to immune complexes | cleared from blood by reticuloendothelial system |
| example of TIII HSR | systemic lupus erythematosus (SLE), where immune complexes usually deposit anywhere but mainly the kidney |
| TIV HSR/ delayed type hypersensitivity | antibody independent, T cell mediated type of immunity |
| how is TIV HSR initiated | by antigen activated T cells (CD4/ CD8 ) |
| when does TIV HSR occur | hours or days after exposure |
| example of TIV HSR/ delayed type hypersensitivity | MS |
| hyperacute rejection | irreversible reaction within minutes/ hours after transplantation (TII HSR) |
| acute rejection | reversible reaction occurring usually within days or weeks after transplant- most common type (TII/IV HSR) |
| types of rejection | hyperacute, acute, and chronic |
| how can acute rejection be treated | immunosuppressive therapy eg cyclosporine |
| how does acute rejection work | dendritic cell in donated organ has MHC 1&2. CD4 reacts against non-self MHC 2 and differentiate into Th1. Th1 makes INF-y and activate macrophages for tissue destruction |
| chronic rejection | irreversible reaction occurring over months to years usually in patients that have survived acute rejection due to immunosuppression therapy |
| how does chronic rejection work | the delayed hypersensitivity reaction involving CD4 cells finally occurs |
| graft vs host | immunocompetent T cells in donor graft recognise recipient antigens as foreign and react against them |
| what has to happen for graft vs host to occur (3) | donor graft must have immunocompetent T cells, recipient must be immunocompromised, and recipient must have MHC antigens that are foreign to donor T lymphocytes |
Created by:
kablooey
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