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Lecture 2                                                     September 11, 2006

Immunology Overview                                   Reading: pg. 71-109

  • Innate vs. adaptive (fig 9.1, fig 9.2, pg. 71
  • Exterior defenses (fig. 9.3, pg. 72)
  • Phagocytes (fig. 9.11, pg. 75)
    • Macrophages (fig. 9.21, pg. 81)
    • Polymorphonuclear granulocytes
  • Antimicrobial mechanisms
    • Oxygen independent
    • Oxygen dependent
  • Complement system (fig. 9.14, pg. 77, fig. 9.22, pg. 81)
  • Acute phase proteins
    • C-reactive proteins
    • Interferon
  • Extracellular killing
    • Natural killer cells (fig. 9.29, pg. 84)
    • eosinophils
  • Acute inflammatory response (fig. 9.31, pg. 85)
    • Role of antibodies (immunoglobulins)
  • Major immunoglobulin classes (fig. 10.2, pg. 89)
  • T lymphocytes (fig.10.11, pg. 93)
  • B lymphocytes
    • Antibody production
    • Memory cells
  • Lymphocyte stimulation (fig. 11.9, pg. 104, fig. 11.10, fig. 11.11, pg.105, fig. 11.12, pg. 106)
  • Cytokines
  • Regulatory mechanisms
  • Tolerance mechanisms

Immunology Review

p. 71-109

Innate and adaptive immune defenses

p   Innate (Nonspecific) defenses: natural immunity

p   Adaptive (Specific) defenses: protection that develops over organism’s life

Innate immune defenses

p   First line of defense

p   Anatomical barriers – prevent entry

n   skin and mucous membranes

p  Provide physical separation

p  Membranes bathed in antimicrobial secretions

§    mucus
§    sweat - lactic acid and fatty acids
§    lysozyme

n   Normal flora

Adaptive immune response

p   First response - primary response

n   May take a week or more to develop

p   secondary response

n   immune system remembers pathogen on subsequent exposure

n   due to memory cells

 

 

Exterior defenses

Defenses after microbe enters body

p           Defensive strategies

–           Phagocytes

–           Soluble chemical factors (bactericidal enzymes)

Phagocytosis

Macrophages

–      effective against pathogens that live within host cells

–      Fig. 9.21

 

Polymorphonuclear granulocytes

–     Neutrophils

–     Effective against pyogenic (pus-forming) bacteria

–    Primary azurophilic granule - contain myeloperoxidase, lysozyme and cationic proteins

–    Secondary “specific” granules contain lactoferrin and lysozyme

–    Tertiary granules contain lysozyme and acid hydrolases

 

Antimicrobial mechanisms

 

Complement system

p   Consists of Serum proteins that are activated in a cascade

 

 

The Complement System

p    Complement activation:

n    Opsonization ŕ phagocytosis

n    Inflammatory response ŕ Macrophage stimulation

n    MAC attack ŕ cytolysis

Acute phase proteins

p   released as a result of infection or tissue damage

n   C-reactive proteins (CRP)

p  Reacts with cell wall components of bacteria

p  Activates phagocytosis and complement

n   Interferon

p  Antiviral cytokine

p  Inhibit viral RNA translation

p  Prevent spread

Extracellular killing

p   Natural Killer cells

n   Cytotoxic cells that kill virus-infected cells

p   Fig 9.29

Extracellular killing

p   Eosinophils

n   Act against large parasites (helminths)

n   by release of granule contents

p  Major basic protein (MBP)       damage parasite

p  Cationic protein                             membrane

p  Peroxidase

p  Perforin-like molecule  ŕ “leaky pores”

p  Oxygen metabolites ŕ “chemical burns”

 

Acute inflammatory response

Adaptive defenses

p   Specific for each invading microbe

p   Acquired throughout one’s lifetime

p   Involve T and B lymphocytes

p   Divided into

n   Humoral immunity

p  Due to soluble factors

p  Eliminates extracellular pathogens

n   Cellular immunity

p  Mediated by cells

p  Eliminates intracellular pathogens

Antibody

p    Immunoglobulins synthesized by B lymphocytes

p    Structure

Role of antibodies (immunoglobulins)

p    Recognize, bind to and neutralize microbe

p    Ag-Ab complexes

n    Activates complement

p   Opsonization ŕ phagocytosis

p   Acute inflammatory response

Acute Inflammatory Response

n    Also initiated by binding of antibodies (IgE) to mast cells

Major immunoglobulin classes

p   divided based on constant region

T lymphocytes

p   Defend against intracellular pathogens

p   a.k.a T cells - Mediate cellular immunity

n   Matures in thymus

n   Divided into 2 subsets

p  Cytotoxic T cells

p  Helper T cells

T lymphocytes

T lymphocytes

p   Ag enters body, is phagocytized and processed by macrophages

n   macrophages present a portion on surface

p  Macrophages are antigen-presenting cells (APC)

p   Processed Ag combines with specific TH

p   APC releases substances to activate TH cell

p   TH cell activates B cells to divide and differentiate

n   Produce plasma cells and memory B cells

B lymphocytes

p   a.k.a B cells - Mediate humoral immunity

n   Develops in bone marrow

n   proliferate into plasma cells

p  production and secretion of one specific Ab

n   produce memory cells (Fig. 11.9)

 

Lymphocyte stimulation

p   T lymphocytes:

n   Recognize and are activated by antigens on surface of antigen presenting cells (APCs)

 

Lymphocyte stimulation

p   B cells stimulation without help of T cells

Lymphocyte stimulation

p   Stimulation only with help of T helper cells

Cytokines

p   Chemical messengers

p   allow communication between components of immune response

n   Chemokines

p  attract cellular components to specific sites of inflammation

Regulatory mechanisms

p   Regulate expansion of dividing lymphocytes

n   Immune system is antigen driven

n   Antibodies produce negative feedback to down-regulate immune response

 

Tolerance mechanisms

p   To avoid reaction with self molecules:

n   Eliminated by clonal deletion

n   Made anergic (unresponsive) to self antigens

n   Silenced through lack of help from T helper cells or T suppressor cells