Hypersensitivities/ Infections “The Immune System Gone Bad”

Presentation on theme: "Hypersensitivities/ Infections “The Immune System Gone Bad”"— Presentation transcript:

1 Hypersensitivities/ Infections “The Immune System Gone Bad”

2 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

3 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

4 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

5 Sometimes beneficial to host – IgE-mediated destruction of parasites

6 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

7 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)

8

9 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).

10 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

11

12 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

13 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

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

15 Can be life threatening, so individuals should be aware Skin tests – injection – see wheal and flare Lab tests for circulating IgE

16 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)

17 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

18

19 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”)

20

21 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

22

23

24 Systemic lupus erythematosus SLE Autoanitbodies against nucleic acids and other self components

25 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

26 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

27

28

29 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