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  1. 1. PowerPoint to accompanyFoundations in Microbiology Fifth Edition Talaro Chapter 17 Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
  2. 2. Disorders in Immunity Chapter 17 2
  3. 3. Immunopathology• Allergy, hypersensitivity – an exaggerated, misdirected expression of immune responses• Involves the same types of immune reactions as those at work in protective immunities.• Autoimmunity – abnormal responses to self Ag• Immunodeficiency – deficiency or loss of immunity• Cancer – results from a lack of surveillance 3
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  6. 6. Type I Hypersensitivity• Atopy – any chronic local allergy such as hay fever or asthma• Anaphylaxis – a systemic, often explosive reaction that involves airway obstruction and circulatory collapse 6
  7. 7. Mechanism of Type I• sensitizing dose – on first contact with allergen, specific B cells form IgE which attaches to mast cells and basophils• provocative dose - subsequent exposure with the same allergen binds to the IgE-mast cell complex• degranulation releases mediators with physiological effects such as vasodilation and bronchoconstriction• symptoms are rash, itching, redness, increased mucous discharge, pain, swelling, and difficulty breathing 7
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  9. 9. Role of Mast Cells & Basophils• Mast cells are located in the connective tissue of virtually all organs; high conc. in lungs, skin, GI and genital tract• Basophils circulate in blood, migrate into tissues• each cell can bind 10,000-40,000 IgE• cytoplasmic granules contain physiologically active cytokines, histamine, etc• cells degranulate when stimulated by allergen9
  10. 10. Chemical mediators 10
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  12. 12. Systemic Anaphylaxis• Sudden respiratory and circulatory disruption that can be fatal in a few minutes• Allergen and route are variable• Bee stings, antibiotics or serum injection 12
  13. 13. Strategies for circumventing allergic attacks 13
  14. 14. Blocking Ab 14
  15. 15. Type II Hypersensitivity• Reactions that lyse foreign cells• Involve antibodies, complement, leading to lysis of foreign cells• Transfusion reactions – ABO blood groups – Rh factor – hemolytic disease of the newborn 15
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  20. 20. Type III Hypersensitivity• A large quantity of soluble foreign Ag stimulates Ab that produce small, soluble Ag-Ab complexes• Immune complexes become trapped in tissues & incite a damaging inflammatory response – Arthus reaction – local reaction to series of injected Ag to same body site – Serum sickness – systemic disease resulting from repeated injections of foreign proteins 20
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  22. 22. Autoimmunity• In certain type I & II hypersensitivities, the immune system has lost tolerance to self molecules and forms autoantibodies and sensitized T cells against them.• More common in females• Disruption of function can be systemic or organic specific – Systemic lupus erythematosus – Rheumatoid arthritis – Endocrine autoimmunities – Myasthenia gravis – Multiple sclerosis 22
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  27. 27. Type IV Hypersensitivity• Cell-mediated• A delayed response to Ag involving activation of and damage by T cells• Delayed allergic response – skin response to allergens – tuberculin skin test, contact dermititis from plants, metals, cosmetics• Graft rejection – reaction of cytotoxic T cells directed against foreign cells of a grafted tissue; involves recognition of foreign HLA 27
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  31. 31. Immunodeficiency diseases• Components of the immune response system are absent. Deficiencies involve B and T cells, phagocytes, and complement – Primary immunodeficiency – genetically based congenital lack of B-cell and/or T cell activity – B cell defect – agammaglobulinemia – patient lacks antibodies – T cell defect – thymus is missing or abnormal – Severe combined immunodeficiency - both limbs of lymphocyte system are missing or defective; no adaptive immune response – Secondary (acquired) immune deficiency – due to damage after birth (infections, drugs, radiation) AIDS 31
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  33. 33. Cancer• Overgrowth of abnormal tissue arises due to malfunction of immune surveillance• Tumors may be benign (nonspreading) or malignant (a cancer) that spreads from tissue of origin to other sites• Malignant tumors may be – carcinomas originate from epithelial tissue – sarcomas originate from embryonic connective tissue• Cancers occur in nearly every cell type 33
  34. 34. Characteristics of cancerous growths• Disorganized behavior and independence from surrounding normal tissues• Permanent loss of cell differentiation• Expression of special markers on their surface 34
  35. 35. Interrelationship between genes and cancer1. Cancer cell often have damaged chromosomes2. A specific alteration in a gene can lead to cancer3. Predisposition for some cancers is inherited4. Rates of cancer are highest in individuals who cannot repair damaged DNA5. Mutagenic agents cause cancer6. Cells contain genes that can be transformed to cancer-causing oncogenes7. Tumor-supressor genes exist in the normal genome 35
  36. 36. Mechanism of Cancer• Some type of gene alteration turns a normal gene (proto-oncogene) that regulates the onset of mitosis into an oncogene• The oncogene overrides normal mitotic controls and cause the cell to divide continuously• Tumor suppressor genes may be missing or inactivated 36
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  38. 38. Role of viruses in cancer• Some viruses carry oncogenes whose products cause transformation of host cells into cancer cells• Viral genome may be inserted into regulatory sites• Human papillomavirus cervical cancer• Epstein-Barr virus – Burkitt’s lymphoma 38
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  41. 41. Function of immune system in cancer• Cells with cancer-causing potential arise constantly in the body but the immune system normally discovers and destroys them• Cell-mediated immunity, TC, NK & macrophages, antibodies• Immune system fails in cancer – may not be immunogenic enough – may retain self-markers and not be targeted• Maybe a slight or transient failure allows cancer to develop 41