Immunity and Abnormal Responses by hcj

VIEWS: 0 PAGES: 54

									    Chapter 3

   Immunity and
Abnormal Responses

  Dr. Ken Nelson
             THE IMMUNE RESPONSE
• Antigens
   • Self
      • HLA proteins label cells of the individual.
      • Immune system ignores “self” cells.
   • Non-self
      • Immune system recognizes specific non-self antigens
        as foreign.
      • Development of a specific response to that particular
        antigen
      • Memory cells produced to respond quickly to antigen
                  TYPES OF IMMUNITY

• Humoral immunity: Antibodies are produced to protect
  body.
• Cell-mediated immunity (CMI): Lymphocytes are
  programmed to attack non-self cells to protect the
  body.
                    COMPONENTS OF
                   THE IMMUNE SYSTEM
• Lymphoid structures
   • Lymph nodes
   • Spleen
   • Tonsils
   • Intestinal lymphoid tissue
   • Lymphatic circulation
• Immune cells
   • Lymphocytes
   • Macrophages
    COMPONENTS OF THE IMMUNE SYSTEM
               (CONT’D)
• Tissues – immune cell development
   • Bone marrow
      • Origination of immune cells
   • Thymus
      • Maturation of immune cells
STRUCTURES OF THE IMMUNE SYSTEM
                ANTIGENS (IMMUNOGENS)

• Usually exogenous substances
• Cell surface antigens
   • Proteins
   • Polysaccharides
   • Glycoproteins
                               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
       • i.e., monokines and interleukins
   • Present throughout the body
        DEVELOPMENT OF
CELLULAR AND HUMORAL IMMUNITIES
                        CELLS
• Lymphocytes
  • T-lymphocytes
     • From bone marrow stem cells
     • Further differentiation in thymus
     • CMI
     • Cytotoxic T-killer cells
     • Helper T cells
     • Memory T cells
                         CELLS (CONT’D)
• 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
           ANTIBODIES/IMMUNOGLOBULINS
• IgG
  • Most common in blood
• IgM
  • First to increase in immune response
• IgA
  • In secretions
        • Tears
        • Saliva and mucous membranes
        • Colostrum
  ANTIBODIES/IMMUNOGLOBULINS (CONT’D)

• IgE
  • Allergic response
  • Causes release of histamine and other chemicals
  • Results in inflammation
• IgD
  • Attached to B cells
  • Activates B cells
               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
                 CHEMICAL MEDIATORS

• Involved in inflammation and immune reactions
   • i.e., histamine, interleukins
• Variety of functions
   • Signaling
   • Causing cellular damage
                   DIAGNOSTIC TESTS

• Titer (titre)
    • Measures levels of serum immunoglobulins
• Indirect Coombs test
    • Detects Rh blood incompatibility
• Elisa
    • Detects for HIV antibodies
    • Used for a number of other diseases
• MHC typing
    • Tissue matching before transplant procedures
                        IMMUNITY

• Natural immunity
   • Species specific
• Innate immunity
   • Gene specific
   • Related to ethnicity
                   IMMUNITY (CONT’D)

• Primary response
   • First exposure to antigen
   • 1 to 2 weeks for antibody titer to reach efficacy
• Secondary response
   • Repeat exposure to the same antigen
   • More rapid response with efficacy in 1 to 3 days
PRIMARY AND SECONDARY
  IMMUNE RESPONSES
                               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
                     IMMUNITY (CONT’D)
• 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
TYPES OF ACQUIRED IMMUNITY
              TISSUE AND ORGAN
            TRANSPLANT REJECTION
• Hyperacute rejection
   • Immediately after transplantation
• Acute rejection
   • Develops after several weeks
• Chronic/late rejection
   • Occurs after months or years
                 IMMUNOSUPPRESSION

• Reduction of immune response to prevent rejection
• Commonly used drugs
   • Cyclosporine, azathioprine, prednisone
• High risk of infection
   • Due to immune suppression
   • Opportunistic organisms
              HYPERSENSITIVITY REACTIONS
• Type I hypersensitivity – allergic reactions
    • Common
        • Due to allergen
        • Skin rashes
        • Hay fever
    • Causative mechanism
        • Exposure to allergen
        • Development of IgEs
        • Mast cells
    • Complications
        • Anaphylaxis
    HYPERSENSITIVITY REACTIONS (CONT’D)

   Type I hypersensitivity – allergic reactions
    (Cont’d)
     Hay fever/allergic rhinitis
       • Nasal mucosa
     Food allergies
       • Digestive tract mucosa
     Atopic dermatitis/eczema
       • Skin
     Asthma
       • Bronchial mucosa
TYPE I HYPERSENSITIVITY
        ANAPHYLAXIS/ANAPHYLACTIC SHOCK
• Severe, life-threatening
• Systemic hypersensitivity reaction
• Decreased blood pressure due to release of histamine
• Airway obstruction
• Severe hypoxia
• Can be caused by:
   • Latex materials
   • Insect stings
   • Nuts or shellfish; various drugs
                 ANAPHYLAXIS (CONT’D)
• 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
EFFECTS OF ANAPHYLAXIS
SIGNS AND SYMPTOMS OF ANAPHYLAXIS
             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
    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
• Example
   • Response to incompatible blood transfusion
TYPE II HYPERSENSITIVITY
               TYPE III –
    IMMUNE COMPLEX HYPERSENSITIVITY
• Antigen combines with antibody
   • Forming immune complexes – deposited in tissue
   • Activation of complement system
• Process causes inflammation and tissue destruction
• Examples:
   • Glomerulonephritis
   • Rheumatoid arthritis
TYPE III – IMMUNE COMPLEX REACTION
           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
 TYPE IV – CELL-MEDIATED
DELAYED HYPERSENSITIVITY
POISON OAK – TYPE ?? RESPONSE
         AUTOIMMUNE DISORDERS
• Development of antibodies against own cells/tissues
• Auto-antibodies 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; myasthinia gravis;
     scleroderma; pernicious anemia
THE AUTOIMMUNE PROCESS
  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
 “BUTTERFLY RASH”
ASSOCIATED WITH SLE
                         SLE

• Large number of circulating auto-antibodies
   • Against DNA, platelets, erythrocytes…
• Formation of immune complexes
   • Deposited into tissues
• Inflammation and necrosis
• Vasculitis develops in many organs.
   • Impairing blood supply to the tissues
                         SLE (CONT’D)
• Sings and symptoms vary due to organ involvement but
  commonly include:
   • Arthralgia, fatigue, and malaise
   • Cardiovascular problems
   • Polyuria
• Diagnostic test
   • Serum antibodies; LE cells; other blood work
• Treatment
   • Usually treated by a rheumatologist
   • Prednisone (glucocorticoid)
   • Non-steroidal anti-inflammatory drugs
COMMON MANIFESTATIONS OF SLE
                   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 immune deficiencies
   • Loss of the immune response due to specific causes
   • Can occur at any time during the lifespan
       • Infections, splenectomy, malnutrition, liver disease,
         immunosupressant drugs, radiation, chemotherapy
         (cancer)
         IMMUNODEFICIENCY (CONT’D)

• Predisposition to the development of opportunistic
  infections
   • Caused by normal flora
• Usually difficult to treat due to immunodeficiency
• Prophylactic antimicrobial drugs may be used prior to
  invasive procedures
 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
                      AIDS (CONT’D)
• HIV positive
   • Virus is known to be in the body.
   • No evidence of immune suppression
• AIDS
   • Marked clinical symptoms, multiple complications
• Individual is often identified as HIV positive before the
  development of AIDS.
   • Current therapies start if HIV infection is diagnosed
     in the early stages.
 STAGES IN THE DEVELOPMENT OF AIDS




The AIDS virus takes over the machinery of the T cells it infects,
              using the cells to make new viruses.
                  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

								
To top