Hypersensitivities/ Infections

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Hypersensitivities/ Infections

• The Immune System Gone Bad

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Hypersensitivities

1. Allergies Exaggerated immune response against
   environmental antigens
2. Autoimmunity immune response against hosts own
   cells
3. Alloimmunity immune response against beneficial
   foreign tissues, such as transfusions or
   transplants

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These immune processes initiate inflammation and
destroy healthy tissue. Four types Type I
IgE-mediated allergic reactions Type II
tissue-specific reactions Type III
immune-complex-mediated reactions Type IV -
cell-mediated reactions
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Type I - IgE-mediated allergic reactions or
immediate hypersensitivity Characterized by
production of IgE Most common allergic
reactions Most Type I reactions are against
environmental antigens - allergens
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Sometimes beneficial to host IgE-mediated
destruction of parasites
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Selected B cells produce IgE Need repeated
exposure to large quantities of allergen to
become sensitized IgE binds by Fc end to mast
cells after first exposure
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Second exposure (and subsequent exposures)
antigen binds with Fab portion of antibody on
mast cells, and cross-links adjacent antibodies,
causing mast cell to release granules. Response
is immediate ( 5- 30 minutes)
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Histamine release

• Increases vascular permeability, causing edema
• Causes vasodilation
• Constricts bronchial smooth muscle
• Stimulates secretion from nasal, bronchial and
  gastric glands
• Also hives (skin), conjunctivitis (eyes) and
  rhinitis (mucous membranes of nose).

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Late phase reaction

• 2 8 hours lasts for 2 - 3 days
• Other mediators that take longer to be released
  or act
• Chemotactic factors for eosinophils and
  neutrophils
• Leukotrienes
• Prostaglandins
• Protein-digesting enzymes

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Treatment

• First wave antihistamines or epinephrine
  (blocks mast cell degranulation)
• Second wave corticosteroids and nonsteroidal
  anti-inflammatory agents that block synthesis of
  leukotrienes and prostaglandins
• Desensitization by repeated injections of
  allergen formation of IgG

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Anaphylaxis Type I allergic reaction may be
localized or general immediate within a few
minutes of exposure Systemic anaphylaxis pruri
tus(intense itching) urticaria
(hives) Wheezing dyspnea swelling of the
larynx Give epinephrine
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Anaphylactic shock

• Hypotension, edema (esp. of larynx), rash,
  tacycardia, pale cool skin, convulsions and
  cyanosis
• Treatment
• Maintain airway
• Epinephrine, antihistamines, corticosteroids
• Fluids
• Oxygen

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Can be life threatening, so individuals should be
aware

• Skin tests injection see wheal and flare
• Lab tests for circulating IgE

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Type II Tissue specific reactions(antibody-depe
ndent cytotoxicity)

• Most tissues have specific antigens in their
  membranes expressed only by that tissue
• Antibodies bind to cells or surface of a solid
  tissue (glomerular basement membrane)

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Destruction of tissue occurs

• Destruction by Tc Cells which are not antigen
  specific
• Complement-mediated lysis
• Phagocytosis by macrophages(frustrated
  phagocytosis)
• Binding of antibody causes cell to malfunction

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Type III Immune-complex-mediated reactions

• Caused by antigen-antibody complexes formed in
  circulation and deposited in vessel walls or
  other tissues
• Not organ specific
• Effects caused by activation of complement
  chemotaxis of neutrophils
• Neutrophils release lysosomal enzymes into
  tissues (frustrated phagocytosis)

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Type IV- Cell- mediated reactions

• Sensitized T lymphocytes either Tc Cells or
  lymphokine producing Td cells
• Takes 24 72 hours to develop
• Damage by Tc Cell or inflammatory response by Td
  Cells (lymphokines)
• Graft rejection, tumor rejection, TB reaction,
  poison ivy and metal reactions
• Immune diseases
• Tissue rejection

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Systemic lupus erythematosus SLE Autoanitbodies
against nucleic acids and other self components
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Infection - viral

• Viruses extremely small can infect bacteria
• Usually just composed of DNA (or RNA) protein
  coat or capsid
• Cant reproduce on their own need to use a host
  cell

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Infection

• Adsorbed to host cell receptor
• Penetration
• Coat removal
• Uses host enzymes to replicate nucleic acid and
  proteins
• New viruses are assembled
• Virus is released
• Lytic cycle

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Cellular effects

• Decreased synthesis of host proteins
• Disruption of lysosomal membranes
• Changes in host cell membrane proteins
• Transform into cancer cell
• Tissue damage may promote bacterial infection