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Inflammation and Hypersensitivity

Inflammation and Hypersensitivity. I. Now that we know basics about varying forms of cellular and humoral cascades, ready to talk more about dysfunction. A. Inflammation can be cellular mediated and/or humoral and can involve complement and clotting cascade

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Inflammation and Hypersensitivity

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  1. Inflammation and Hypersensitivity

  2. I. Now that we know basics about varying forms of cellular and humoral cascades, ready to talk more about dysfunction • A. Inflammation can be cellular mediated and/or humoral and can involve complement and clotting cascade • B. Text goes over varying complement pathways, can be classical or alternative.

  3. Players in responses • The palyers are the same essentially as in blood section and immuno section

  4. These are usually first to inflammation Both in serum and mucosal, will function much as macrophages

  5. Macrophages are later arriving

  6. Monocytes are close relatives and are more plasma oriented

  7. But much of symptomology comes from these As they release 5HT and histamines and ECP-A

  8. These are usually last even after macros. So if see probably chronic condition

  9. Inflammation has a few aspects • Is based usually on a response to parasites (may be how it evolved) • Uses IgEs a lot and mast cells and eosinophiles • May also use complement • If long term can encapuslate using clotting cascade

  10. Now Hypersensitivity • Four types: • I- IgE mediated by allergen • II-tissue specific • III-immune complex • IV-cell-mediated

  11. Type I • Big Player is histamine which has opposing effects based on which subtype of receptor is activated. • H1 tend to increase inflammation • H2 tend to ameliorate • H3 are more CNS derived

  12. Histamine Receptors H1 Immune recruitment Bronchial constriction G-pr- IP3 H2 cAMP Immune silencing via Ts Gastric secretion

  13. Allergy response Allergen sensitization IgE Masteosins H1

  14. II HLA mismatch CD8 MHCII Attack complex

  15. Mechanisms of anti self • Phagocytosis after opsinization • Complementation • Tc destruction • Ab blockade of receptor subtypes

  16. III allergen complexation Attack complex

  17. IV Antigen presenting cell destroyed either directly or after antigen presentation by host antigen CD4 or CD8 If CD4 termed delayed

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