hypersensitivities/ infections “the immune system gone bad”
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Hypersensitivities/ Infections
“The Immune System Gone Bad”
Hypersensitivities
1. Allergies – Exaggerated immune response against environmental antigens
2. Autoimmunity – immune response against host’s own cells
3. Alloimmunity – immune response against beneficial foreign tissues, such as transfusions or transplants
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
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
Sometimes beneficial to host – IgE-mediated destruction of parasites
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
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)
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).
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
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
Anaphylaxis – Type I allergic reaction
may be localized or general
immediate – within a few minutes of exposure
Systemic anaphylaxis:pruritus(intense itching)urticaria (hives)Wheezing; dyspnea; swelling of the larynx
Give epinephrine
Anaphylactic shock
• Hypotension, edema (esp. of larynx), rash, tacycardia, pale cool skin, convulsions and cyanosis
• Treatment:– Maintain airway– Epinephrine, antihistamines, corticosteroids– Fluids– Oxygen
Can be life threatening, so individuals should be aware
• Skin tests – injection – see wheal and flare
• Lab tests for circulating IgE
Type II – Tissue specific reactions(antibody-dependent 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)
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
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”)
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
Systemic lupus erythematosus SLE
Autoanitbodies against nucleic acids and other self components
Infection - viral
• Viruses extremely small – can infect bacteria
• Usually just composed of DNA (or RNA) + protein “coat” or capsid
• Can’t reproduce on their own – need to use a host cell
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
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
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