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

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

Innate Defenses

The immune system protects the body from pathogens through two main types of defenses: innate (nonspecific) and adaptive (specific). Innate defenses provide immediate, general protection, while adaptive defenses target specific threats.

Surface Barriers: The First Line of Defense

  • Skin: A highly keratinized epithelial membrane that acts as a physical barrier to most microorganisms, their enzymes, and toxins.

  • Mucous Membranes: Line body cavities open to the exterior, trapping pathogens and preventing their entry.

  • Protective Chemicals:

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

    • Enzymes (Lysozyme): Destroy microorganisms (found in saliva, tears, mucus).

    • Mucin: Forms sticky mucus to trap pathogens.

    • Defensins: Antimicrobial peptides that disrupt microbial membranes.

    • Other Secretions: Specialized regional secretions (e.g., sebum, sweat) with antimicrobial properties.

Surface Membrane Barrier

Protective Function

Skin

Physical barrier; acidic secretions inhibit bacteria

Mucous Membranes

Trap pathogens; contain lysozyme and mucin

Defensins

Antimicrobial peptides

Acid

Inhibits bacterial growth

Enzymes

Destroy microorganisms

Innate Internal Defenses: The Second Line of Defense

  • Phagocytes:

    • Neutrophils and Macrophages engulf and destroy pathogens.

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

    • Destruction occurs via engulfment, acidification of phagolysosome, and digestion with lysosomal enzymes.

    • If unable to ingest, phagocytes may release lethal chemicals.

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

  • Inflammation:

    • Triggered by injury, infection, or irritants.

    • Benefits: Prevents spread of damage, disposes of debris/pathogens, alerts adaptive immunity, initiates repair.

    • Cardinal Signs: Redness, heat, swelling, pain.

    • Caused by release of inflammatory chemicals (e.g., histamine, kinins, prostaglandins) leading to vasodilation and increased capillary permeability.

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

  • Antimicrobial Proteins:

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

    • Complement: Group of ~20 plasma proteins; destroy pathogens via classical, lectin, and alternative pathways.

  • Fever:

    • Systemic response to infection.

    • Pyrogens (from leukocytes/macrophages) act on hypothalamus to raise body temperature.

    • Higher temperature inhibits bacterial growth and enhances repair.

Inflammatory Chemical

Role

Histamine

Vasodilation, increased permeability

Kinins

Vasodilation, pain induction

Prostaglandins

Vasodilation, pain, chemotaxis

Complement

Opsonization, cell lysis

Interferons

Antiviral response

Adaptive Defenses

Adaptive immunity is specific, systemic, and has memory. It consists of humoral (antibody-mediated) and cellular (cell-mediated) responses.

Key Aspects of Adaptive Immunity

  • Specificity: Targets specific antigens.

  • Systemic Response: Not limited to infection site.

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

Humoral Immunity

  • Provided by antibodies produced by B lymphocytes in body fluids.

Cellular Immunity

  • Involves direct attack by T lymphocytes; living cells are the protective factor.

Antigens

Antigens are substances that trigger adaptive immune responses. They are recognized as foreign and targeted by the immune system.

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

  • Haptens: Incomplete antigens; not immunogenic unless attached to 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.

B and T Lymphocytes & Antigen-Presenting Cells (APCs)

B and T lymphocytes are central to adaptive immunity. Their development ensures immunocompetence (ability to recognize antigens) and self-tolerance (avoid attacking self).

  • Origin: Both 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 effector and memory cells.

  • APCs:

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

    • Macrophages: Present antigens to T cells, become aggressive phagocytes.

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

Cell Type

Origin

Maturation Site

Main Function

B Lymphocyte

Bone marrow

Bone marrow

Antibody production (humoral immunity)

T Lymphocyte

Bone marrow

Thymus

Cell-mediated immunity

Dendritic Cell

Body surfaces

---

Antigen presentation

Macrophage

Monocytes (blood)

Connective tissue

Phagocytosis, antigen presentation

Humoral Immunity: Antibody Production

Humoral immunity targets extracellular antigens through antibody production by B cells.

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

  • Plasma Cells: Secrete antibodies specific to the antigen.

  • Memory Cells: Provide rapid response upon re-exposure to the same antigen.

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:

    • Naturally Acquired: Infection.

    • Artificially Acquired: Vaccination.

  • Passive Immunity:

    • Naturally Acquired: Maternal antibodies (placenta, breast milk).

    • Artificially Acquired: Injection of preformed antibodies.

Antibody Structure and Classes

  • Antibody (Immunoglobulin) Structure: Y-shaped molecule with variable regions for antigen binding.

  • Functions: Neutralization, agglutination, precipitation, complement activation.

  • Five Classes:

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

    • IgA: Found in mucous membranes, saliva, tears; protects body surfaces.

    • IgD: Functions as B cell receptor.

    • IgG: Most abundant; crosses placenta; provides passive immunity to fetus.

    • IgE: Involved in allergic reactions and defense against parasites.

Immunoglobulin Class

Main Function

IgM

Primary response, complement activation

IgA

Protects mucosal surfaces

IgD

B cell receptor

IgG

Secondary response, crosses placenta

IgE

Allergy, parasite defense

Mechanisms of Antibody Action

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

  • Agglutination: Antibodies cause pathogens to clump together.

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

  • Complement Activation: Antibody-antigen complexes activate complement, leading to cell lysis.

Key Equations

  • Antibody Titer (Concentration):

Example

  • Vaccination: Artificially acquired active immunity; stimulates production of memory cells for rapid response upon exposure to the pathogen.

  • Maternal Antibodies: IgG crosses placenta, providing passive immunity to the newborn.

Additional info: Adaptive immunity relies on genetic recombination in lymphoid stem cells to generate diverse antigen receptor sites, enabling recognition of a vast array of pathogens.

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