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Chapter 15- Hypersensitivities

Chapter 15- Hypersensitivities. Where we’re going Four types of hypersensitivities Spend particular time on type I- allergies- and type IV- dth. Some more cell signaling. Fairly clinical, and micro students have seen some of this before. Type I hypersensitivity- allergies, asthma, etc.

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Chapter 15- Hypersensitivities

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  1. Chapter 15- Hypersensitivities Where we’re going • Four types of hypersensitivities • Spend particular time on type I- allergies- and type IV- dth. • Some more cell signaling. • Fairly clinical, and micro students have seen some of this before.

  2. Type I hypersensitivity- allergies, asthma, etc. • One of the earliest immune response observations- dogs dying when vaccinated against jellyfish toxins! • One of the last to actually be discovered. • Localized: hay fever, asthma • Systemic-anaphylaxis

  3. The big Q is: why this particular response, and not IgG or A?? WE have TONS of mast cells! 104/mm3!

  4. The discovery of IgE: P-K reaction is a wheal and flare at the site of the test. In this test, Serum was injected into a non-Atopic individual for the test (not sure it would pass IRB today)

  5. Things that trigger mast cell degranulation. Only the first one is clinical.

  6. Multiple activations: PTK, adenyl cyclase, PL methylation Membrane alteration brings in Ca++ 2 main results- degranulation& PG/LT production Note that the players are similar: cAMP, ITAMS, DAG and IP3, PKC, Ca++,

  7. The small molecules- histamine, PG/LT’s, will work early; the chemotactic factors and cytokiines will work later.

  8. Asthma- early phase and late phase response. Early is due to histamines, PG’s, LT’s; late due to cytokines released by mast cells and Th2 cells- neutrophil and eosinophil infiltration, resulting in damage.

  9. Control- drugs & hyposensitization • Control: Most of it is by drugs- antihistamines, steroids, that block specific parts of the response. (Table 16-4) • Hyposensitization- try to get an IgG instead of an IgE response.

  10. IL4-IFN gamma story • IL-4 increases this response, IFN decreases. Th1 response decreases, Th2 increases.- This is one theory about the rise in asthma in developed countries. As the frequency of viral URT's and TB decreases in developed countries, the lungs may end up with more Th2 than Th1 cells, thus producing an IgE response instead of a cell-mediated response.

  11. These are in vitro assays- cultured plasma cells treated w/ IL-4 or IFN gamma

  12. IgE assays- low amts mean we need to use radioactivity

  13. RIST- radioimmunosorbent test- total IgE

  14. RAST- radioallergosorbent test- specific IgE

  15. Moving right along- Type II • We produce IgG that reacts to cells, often RBC’s, as antigens. • ADCC or complement-mediated cell lysis. • Hemolytic disease of the newborn

  16. Don’t have to learn- just a cool slide! One sugar extra makes you A,B, or AB

  17. Rh- mom, Rh+ baby

  18. Type III- immune complex • Large amts of Ab-Ag complexes- activate complement, mast cell degranulation, neutrophil recruitment, followed by tissue damage-Arthus reaction • Generalized- serum sickness, autoimmune disease; the complexes are deposited in joints, kidney, other tissues.

  19. Type IV- delayed type hypersensitivity • Cell mediated • Think poison ivy, Tb test, contact dermatitis • Seems to be an obnoxious form of the same rxn that protects us from TB.

  20. You’re a dead mouse w/o IFNgamma!

  21. Cytokines produced attract MORE mphages- contribute to the damage.

  22. Things to know from Ch 15 • Four types of Hypersensitivities • Mast cell trigger- • Main responses- degranulation, PG/LT response- relation to drugs that control. • Asthma- early and late phase • RIST and RAST • Type II- hemolytic disease of the newborn • Type III- Arthus, serum sickness, glomerulonephritis • Type IV- only one that’s cell mediated; Th1-CD4; mphages roles.

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