Chapter 21: The Immune System – Innate and Adaptive Body Defenses

Innate Defenses

Surface Barriers: The First Line of Defense

The body’s initial protection against pathogens is provided by surface barriers, which include the skin and mucous membranes. These barriers prevent the entry of most microorganisms and their harmful products.

• Skin: A highly keratinized epithelial membrane that acts as a physical barrier to pathogens.

• Mucous Membranes: Line body cavities open to the exterior and trap pathogens.

• Protective Chemicals:

  • Acid: Inhibits bacterial growth (e.g., skin, stomach, vagina).

  • Enzymes: Lysozyme in saliva, tears, and mucus destroys bacteria.

  • Mucin: Forms sticky mucus to trap microorganisms.

  • Defensins: Antimicrobial peptides that disrupt microbial membranes.

  • Other Secretions: Specialized chemicals in various regions (e.g., sebum, sweat).

Internal Defenses: The Second Line of Defense

If pathogens breach surface barriers, internal defenses are activated. These include phagocytic cells, natural killer cells, inflammation, antimicrobial proteins, and fever.

• Phagocytes: Neutrophils and macrophages engulf and destroy pathogens.

  • Pathogens are coated with opsonins (complement proteins) to enhance adherence.

  • Destruction occurs via engulfment, acidification, and lysosomal enzymes.

  • If unable to ingest, phagocytes release lethal chemicals.

• Natural Killer (NK) Cells: Lyse and kill cancer and virus-infected cells; secrete chemicals to enhance inflammation.

• Inflammation: Response to injury or infection; prevents spread, disposes of debris, alerts adaptive immunity, and initiates repair.

  • Four cardinal signs: Redness, heat, swelling, pain.

  • Caused by release of inflammatory chemicals (e.g., histamine, kinins, prostaglandins).

  • Increased capillary permeability allows fluid, antibodies, and clotting factors into tissues.

  • Neutrophils and macrophages migrate to the site via leukocytosis, margination, diapedesis, and chemotaxis.

• Antimicrobial Proteins:

  • Interferons: Produced by virus-infected cells; induce synthesis of antiviral proteins in neighboring cells.

  • Complement: Group of ~20 plasma proteins; destroy pathogens via three activation pathways:

    • Classical pathway: Antibody-dependent.

    • Lectin pathway: Lectin binding to pathogen.

    • Alternative pathway: Direct interaction with pathogen.

• Fever: Systemic response; pyrogens from leukocytes/macrophages act on hypothalamus to raise body temperature.

Adaptive Defenses

Overview of Adaptive Immunity

The adaptive immune system provides specific, systemic, and memory-based defense against pathogens. It consists of humoral and cellular immunity.

• Specificity: Targets specific antigens.

• Systemic Response: Not limited to infection site.

• Memory: Faster, stronger response upon re-exposure.

• Humoral Immunity: Mediated by antibodies produced by B lymphocytes in body fluids.

• Cellular Immunity: Direct attack by T lymphocytes; involves living cells as effectors.

Antigens

Antigens are substances that trigger adaptive immune responses. They are recognized as foreign and provoke the production of specific antibodies or lymphocyte activation.

• Complete Antigens: Possess immunogenicity (stimulate lymphocyte proliferation) and reactivity (react with lymphocytes/antibodies).

• Haptens: Incomplete antigens; not immunogenic alone but can become harmful when combined with body proteins.

• Antigenic Determinants: Specific regions of an antigen recognized by antibodies or lymphocytes.

• Self-Antigens: Body’s own antigens, not antigenic to self; identified by MHC proteins on cell surfaces.

Cells of Adaptive Immunity: B and T Lymphocytes & Antigen-Presenting Cells

B and T lymphocytes are central to adaptive immunity. Their development ensures immunocompetence and self-tolerance. Antigen-presenting cells (APCs) activate T cells by presenting processed antigens.

• Origin: All lymphocytes originate in bone marrow.

• Maturation:

  • B cells: Mature in bone marrow.

  • T cells: Mature in thymus.

• Immunocompetence: Ability to recognize specific antigens.

• Self-Tolerance: Ability to avoid attacking self-antigens.

• Clonal Selection: Antigen binding selects lymphocytes for further development; activated cells divide into clones.

• Effector Cells: Actively fight infection.

• Memory Cells: Provide rapid response upon re-exposure.

• Antigen-Presenting Cells (APCs):

  • Dendritic Cells: Phagocytose antigens, migrate to lymphoid organs, present to T cells.

  • Macrophages: Present antigens to T cells, become more aggressive after activation.

  • B Lymphocytes: Present antigens to helper T cells for full activation.

Humoral Immunity: Antibody-Mediated Response

Humoral immunity involves the production of antibodies by B cells, targeting extracellular antigens. The process includes clonal selection, plasma cell formation, and immunological memory.

• Clonal Selection: Antigen binds to B cell receptors, activating the B cell to proliferate and differentiate.

• Plasma Cells: Secrete antibodies specific to the antigen.

• Memory Cells: Remain for rapid response to future exposures.

Immunological Memory:

• Primary Response: First exposure; lag of 3–6 days; antibody levels peak at ~10 days.

• Secondary Response: Subsequent exposure; rapid (hours), higher antibody levels, longer duration.

Active vs. Passive Humoral Immunity:

• Active Immunity: Body produces antibodies in response to antigen.

  • Naturally Acquired: Infection.

  • Artificially Acquired: Vaccination.

• Passive Immunity: Preformed antibodies are given.

  • Naturally Acquired: Maternal antibodies to fetus.

  • Artificially Acquired: Injection of antibodies from another source.

Antibody Structure and Classes:

• Antibodies (immunoglobulins) are Y-shaped proteins with variable regions for antigen binding.

• Five major classes:

  • IgM: First antibody produced; pentamer; activates complement.

  • IgA: Found in secretions; protects mucosal surfaces.

  • IgD: Functions as B cell receptor.

  • IgG: Most abundant; crosses placenta; activates complement.

  • IgE: Involved in allergic reactions; binds to mast cells and basophils.

Mechanisms of Antibody Action:

• Neutralization: Antibodies block harmful effects of toxins or viruses.

• Agglutination: Antibodies cause clumping of cells.

• Precipitation: Soluble antigens are cross-linked and precipitated.

• Complement Activation: Leads to cell lysis.

Example: Vaccination induces active, artificial immunity by exposing the body to harmless forms of antigens, stimulating antibody production and memory cell formation.

Additional info: The notes above expand brief points into full academic explanations, add definitions, and organize content for exam preparation. Tables are recreated for comparison and classification. All equations and formulas are not directly relevant to this chapter, as immunology is primarily descriptive and mechanistic.