Ch 7

1. Chapter 7
Immunity

2. Immune System
 Responsible for body defenses
 Nonspecific response (defense)
• Examples: phagocytosis, inflammation
 Specific response (defense)
• Production of specific antibodies against foreign
substances
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3. Components of the Immune
System
 Lymphoid structures
 Lymph nodes
 Spleen
 Tonsils
 Intestinal lymphoid tissue
 Lymphatic circulation
 Immune cells
 Lymphocytes
 Macrophages
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4. Components of the Immune
System (Cont.)
 Tissues—immune cell development
 Bone marrow
• Origination of all immune cells
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 Thymus
• Maturation of T lymphocytes

5. Structures of the Immune System
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6. Elements of the Immune System
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 Antigens
 Self
• HLA proteins label cells of the individual.
• Immune system ignores self cells.
 Non-self
• Immune system recognizes specific nonself antigens as
foreign.
• Development of a specific response to that particular
antigen
• Memory cells produced to respond quickly to antigen

7. Antigens (Immunogens)
 Usually exogenous substances
 Cell surface antigens
 Proteins
 Polysaccharides
 Glycoproteins
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8. Cells
 Macrophages
 Initiation of immune response
 Develop from monocytes
 Part of the mononuclear phagocytotic system
 Engulf foreign material
 Display antigens of foreign material
 Secrete chemicals
• Examples: monokines, interleukins
 Present throughout the body
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9. Cells
 Lymphocytes
 T lymphocytes
• From bone marrow stem cells
• Further differentiation in thymus
• Cell-mediated immunity
• Cytotoxic T killer cells
• Helper T cells
• Memory T cells
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10. Cells (Cont.)
 Lymphocytes
 B lymphocytes
• Responsible for production of antibodies
• Humoral immunity
• Mature in bone marrow
 Proceed to spleen and lymphoid tissue
• Plasma cells
 Produce antibodies
• B memory cells
 Can quickly form clone of plasma cells
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11. Types of Immunity
 Humoral immunity: Antibodies are produced
to protect the body.
 Cell-mediated immunity (CMI): Lymphocytes
are programmed to attack nonself cells to
protect the body.
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12. Development of Cellular and
Humoral Immunities
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13. Antibodies and Immunoglobulins
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 IgG
 Most common in blood
 IgM
 First to increase in immune response
 IgA
 In secretions
• Tears
• Saliva and mucous membranes
• Colostrum

14. Antibodies and Immunoglobulins
(Cont.)
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 IgE
 Allergic response
 Causes release of histamine and other chemicals
 Results in inflammation
 IgD
 Attached to B cells
 Activates B cells

15. Review of the Major Components
of the Immune System
 Major components of the immune system and
their function
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16. Complement System
 Activated during immune reactions with IgG
or IgM
 Group of inactive proteins circulating in blood
 C1 to C9
 Causes cell damage and further inflammation
when activated
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17. Chemical Mediators
 Involved in inflammation and immune
reactions
 Examples: histamine, interleukins
 Variety of functions
 Signaling
 Causing cellular damage
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18. Diagnostic Tests
 Titer (titre)
 Measures levels of serum immunoglobulins
 Indirect Coombs’ test
 Detects Rh blood incompatibility
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 Elisa
 Detects HIV antibodies
 Used for a number of other diseases
 MHC typing
 Tissue matching before transplantation
procedures

19. Immunity
 Natural immunity
 Species-specific
 Innate immunity
 Gene-specific
 Related to ethnicity
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20. Immunity (Cont.)
 Primary response
 First exposure to antigen
 1 to 2 weeks before antibody titer reaches efficacy
 Secondary response
 Repeat exposure to the same antigen
 More rapid response, with efficacy in 1 to 3 days
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21. Primary and Secondary Immune
Responses
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22. Immunity
 Active natural immunity
 Natural exposure to antigen
 Development of antibodies
 Active artificial immunity
 Antigen purposefully introduced to body
 Stimulation of antibody production
 Immunization
 Booster immunization
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23. Immunity (Cont.)
 Passive natural immunity
 IgG transferred from mother to fetus:
• Across placenta
• Through breast milk
 Protection of infant for the first few months of life
or until weaned
 Passive artificial immunity
 Injection of antibodies
 Short-term protection
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24. Types of Acquired Immunity
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25. Tissue and Organ Transplant
Rejection
 Hyperacute rejection
 Immediately after transplantation
 Acute rejection
 Develops after several weeks
 Chronic, late rejection
 Occurs after months or years
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26. Immunosuppression
 Reduction of immune response to prevent
rejection
 Commonly used drugs
 Cyclosporine, azathioprine, prednisone
 High risk of infection
 Caused by immunosuppression
 Opportunistic organisms
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27. Hypersensitivity Reactions
 Type I hypersensitivity—allergic reactions
 Common
• Caused by allergen
• Skin rashes
• Hay fever
 Causative mechanism
• Exposure to allergen
• Development of IgEs
• Mast cells
 Complications
• Anaphylaxis
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28. Hypersensitivity Reactions
(Cont.)
 Type I hypersensitivity–allergic reactions
(Cont.)
 Hay fever: allergic rhinitis
• Nasal mucosa
 Food allergies
• Digestive tract mucosa
 Atopic dermatitis/eczema
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• Skin
 Asthma
• Bronchial mucosa

29. Type I Hypersensitivity
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30. Anaphylaxis: Anaphylactic Shock
 Severe, life-threatening
 Systemic hypersensitivity reaction
 Decreased blood pressure caused by release
of histamine
 Airway obstruction
 Severe hypoxia
 Can be caused by:
 Latex materials
 Insect stings
 Nuts or shellfish; various drugs
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31. Anaphylaxis (Cont.)
 Signs and symptoms
 Generalized itching or tingling, especially in oral
cavity
 Coughing
 Difficulty breathing
 Feeling of weakness
 Dizziness or fainting
 Sense of fear and panic
 Edema around eyes, lips, tongue, hands, feet
 Hives
 Collapse with loss of consciousness
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32. Effects of Anaphylaxis
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33. Signs and Symptoms of
Anaphylaxis
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34. Treatment for Anaphylaxis
 Requires first aid response:
 Administer EpiPen if available
 Call 911 (many paramedics can start drug
treatment and oxygen)
 Treatment in emergency department:
 Epinephrine
 Glucocorticoids
 Antihistamines
 Oxygen
 Stabilize BP
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35. Type II: Cytotoxic Hypersensitivity
 Antigen is present on cell membrane
 May be normal body component or exogenous
 Circulating IgGs react with antigen
 Destruction by phagocytosis or cytolytic enzymes
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 Example
 Response to incompatible blood transfusion

36. Type II Hypersensitivity
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37. Type III: Immune Complex
Hypersensitivity
 Antigen combines with antibody
 Forms immune complexes, deposited in tissue
 Activation of complement system
 Process causes inflammation and tissue
destruction
 Examples:
 Glomerulonephritis
 Rheumatoid arthritis
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38. Type III: Immune Complex
Reaction
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39. Type IV: Cell-Mediated or
Delayed Hypersensitivity
 Delayed response by sensitized T lymphocytes
 Release of lymphokines
 Inflammatory response
 Destruction of the antigen
 Examples:
 Tuberculin test
 Contact dermatitis
 Allergic skin rash
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40. Autoimmune Disorders
 Development of antibodies against own cells
or tissues
 Autoantibodies are antibodies formed against
self-antigens—loss of self-tolerance.
 Disorder can affect single organs or tissues
or can be generalized.
 Examples:
 Hashimoto thyroiditis, systemic lupus
erythematosus, rheumatic fever, myasthenia
gravis, scleroderma, pernicious anemia
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41. The Autoimmune Process
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42. Type IV: Cell-Mediated Delayed
Hypersensitivity
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43. Systemic Lupus
Erythematosus (SLE)
 Chronic inflammatory disease
 Affects a number of organ systems
 Characteristic facial rash—“butterfly rash”
 Affects primarily young women
 Incidence is higher in African Americans,
Asians, Hispanics, Native Americans
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44. Butterfly Rash Associated with SLE
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45. SLE
 Large number of circulating autoantibodies
 Against DNA, platelets, erythrocytes
 Formation of immune complexes
 Deposited into tissues
 Inflammation and necrosis
 Vasculitis develops in many organs.
 Impairs blood supply to the tissues
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46. SLE (Cont.)
 Sings and symptoms vary because of organ
involvement but commonly include:
 Arthralgia, fatigue, malaise
 Cardiovascular problems
 Polyuria
 Diagnostic test
 Serum antibodies, LE cells, other blood work
 Treatment
 Usually treated by a rheumatologist
 Prednisone (glucocorticoid)
 Nonsteroidal anti-inflammatory drugs
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47. Common Manifestations of SLE
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48. Immunodeficiency
 Partial or total loss of one or more immune
system components
 Increased risk of infection and cancer
 Primary deficiencies
 Basic developmental failure somewhere in the
system
 Secondary or acquired immunodeficiencies
 Loss of the immune response from specific causes
 Can occur at any time during the life span
• Infections, splenectomy, malnutrition, liver disease,
immunosuppressant drugs, radiation, chemotherapy
(cancer)
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49. Immunodeficiency (Cont.)
 Predisposition to the development of
opportunistic infections
 Caused by normal flora
 Usually difficult to treat because of
immunodeficiency
 Prophylactic antimicrobial drugs may be used
prior to invasive procedures.
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50. Acquired Immunodeficiency
Syndrome (AIDS)
 AIDS—chronic infectious disease caused by
the human immunodeficiency virus (HIV)
 HIV destroys helper T cells—CD4
lymphocytes
 Loss of immune response
 Increased susceptibility to secondary
infections and cancer
 Prolonged latent period
 Development may be suppressed by
antivirals
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51. AIDS (Cont.)
 HIV-positive individual
 Virus is known to be in the body.
 No evidence of immunosuppression
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 AIDS
 Marked clinical symptoms, multiple complications
 Individual often identified as HIV-positive
before development of AIDS
 Current therapies start if HIV infection is
diagnosed in the early stages.

52. Stages in the Development
of AIDS
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53. History of AIDS
 First case recognized in 1979; HIV identified
in 1984
 Evidence of earlier sporadic cases
 Now considered to be a pandemic
 Occurs in men and women
 2006, CDC: 1 million cases in North America
 2007, UN: 33 million cases globally; 22
million of those in sub-Saharan Africa
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