Type III Hypersensitivity

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7 Terms

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Type III Hypersensitivity

Acute inflammation caused by an immune complex with IgM or IgG (formed in fluid) depositing in the body
Activates complement and PMNs, Ag can originate from microbes or self antigens

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Vasculitis

Etiology: Idiopathic or can be associated with Systemic Lupus Erythematosus (SLE)
Inflammation of vascular wall caused by immune complex deposition
Petechiae (red dots) can fuse and cause necrotizing vasculitis

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Vasculitis mechanism

  1. Trigger - Exposure to Ag

  2. Make IgM and IgG (affinity maturation)

  3. Formation of immune complex 1 week after exposure to soluble Ag

  4. Immune complex deposits

  5. Inflammation (activated complement + opsonin for PMNs)

  6. Tissue/cell damage in vessel with hemorrhages → Petechiae

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Arthus Reaction

Inflammation associated with vaccination due to sensitization to vaccine components
Immune complex deposition intradermally in tissue fluid

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Arthus reaction pathogenesis

  1. Pre-formed Abs that can react with vaccine components

  2. Patient vaccinated → Immune complex forms at vaccination site and deposits

  3. Activation of PMNs and complement cascade causing inflammation at injection site

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Staph Marginal Keratitis

Corneal inflammation due to immune complex deposition on cornea
Associated with staph infections

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Staph marginal keratitis pathogenesis

  1. Bacterial conjunctivitis with staph

  2. Staph necrosis by immune system or antibiotics → Release of soluble staph antigens

  3. Immune complex forms with pre-formed Abs and deposits in peripheral cornea stroma

  4. Complement activation and POMN degranulation → Damage cornea

  5. Opacification of inflamed area and formation of marginal ulcer