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

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Overview of the Immune System

Introduction

The immune system protects the body from disease-causing organisms and cancerous cells through a series of defense mechanisms. These mechanisms are categorized into two intrinsic systems: innate defenses and adaptive defenses. Each system has distinct components and functions, working together to provide resistance to disease.

Immune system defense flowchart

Innate (Nonspecific) Defenses

Surface Barriers: Skin and Mucous Membranes

Surface barriers are the body's first line of defense, preventing the entry of pathogens. These include the skin and mucous membranes, which act as physical and chemical barriers.

  • Skin: Provides a tough, keratinized barrier.

  • Mucous membranes: Trap pathogens and contain antimicrobial substances.

  • Secretions: Include acid mantles, enzymes, mucin, defensins, and sebum.

Innate vs adaptive defenses table

Internal Defenses: Cells and Chemicals

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

  • Phagocytes: Neutrophils and macrophages engulf and digest pathogens.

  • Natural Killer (NK) Cells: Destroy infected or abnormal cells by inducing apoptosis.

  • Inflammation: Localized response to injury, characterized by redness, heat, swelling, and pain.

  • Antimicrobial Proteins: Interferons and complement proteins inhibit pathogen replication and promote destruction.

  • Fever: Systemic response to infection, raising body temperature to inhibit pathogen growth.

NK cell mechanism Phagocytosis steps

Phagocytosis

Phagocytosis is a process by which phagocytes ingest and destroy pathogens. The steps include adherence, engulfment, fusion with lysosomes, digestion, and exocytosis of residual material.

  • Adherence: Phagocyte binds to pathogen.

  • Engulfment: Pathogen is enclosed in a phagosome.

  • Fusion: Phagosome fuses with lysosome.

  • Digestion: Lysosomal enzymes break down pathogen.

  • Exocytosis: Residual material is expelled.

Phagocytosis steps

Natural Killer (NK) Cells

NK cells are large lymphocytes that provide immune surveillance. They attack cells lacking self (MHC) surface receptors, releasing perforin and granzymes to induce apoptosis.

  • Perforin: Forms pores in target cell membrane.

  • Granzymes: Enter pores and trigger apoptosis.

NK cell mechanism

Inflammation

Inflammation is a nonspecific response to tissue injury, serving to prevent the spread of damaging agents, dispose of debris, and set the stage for repair. It is characterized by four cardinal signs: swelling, redness, heat, and pain.

  • Stage 1: Release of inflammatory chemicals (histamine, kinins, prostaglandins, cytokines).

  • Stage 2: Vasodilation and increased vascular permeability (causes redness, heat, swelling, pain).

  • Stage 3: Phagocyte mobilization (leukocytosis, margination, diapedesis, chemotaxis).

Inflammation flowchart Tissue injury and healing Inflammation signs Phagocyte mobilization

Antimicrobial Proteins: Interferons and Complement

Antimicrobial proteins play a crucial role in innate immunity. Interferons are released by virus-infected cells to inhibit viral replication. The complement system consists of plasma proteins that enhance both innate and adaptive defenses.

  • Interferons: Block viral protein synthesis and activate NK cells.

  • Complement: Promotes phagocytosis, enhances inflammation, and causes cell lysis.

Interferon mechanism Interferon and NK cell activation Complement system mechanism Complement activation and opsonization Complement opsonization Complement opsonization Complement opsonization Complement opsonization Complement opsonization Complement opsonization Complement opsonization

Fever

Fever is a final nonspecific defense mechanism. It is an abnormally high body temperature induced by pyrogens released from leukocytes and macrophages. Fever inhibits pathogen replication and increases metabolic rate, aiding repair.

  • Pyrogens: Fever-inducing molecules (e.g., interleukins, TNFα).

  • Stages: Onset, stadium, defervescence.

Adaptive (Specific) Defenses

Characteristics of Adaptive Immunity

Adaptive immunity is specific, systemic, and has memory. It involves lymphocytes (B and T cells) and antigen-presenting cells (APCs). Adaptive responses are slower but more effective upon repeated exposure.

  • Antigen-specific: Targets identified pathogens.

  • Systemic: Occurs throughout the body.

  • Memory: Stronger and faster response upon re-exposure.

Humoral Immunity (Antibody-Mediated)

B cells produce antibodies that target extracellular antigens. Antibodies bind to antigens, marking them for destruction by phagocytes or complement.

  • Antibodies: Immunoglobulins (IgM, IgA, IgD, IgG, IgE).

  • Primary response: Initial exposure, slower antibody production.

  • Secondary response: Faster, stronger response due to memory cells.

Cellular Immunity (Cell-Mediated)

T cells defend against intracellular antigens, cancer cells, and foreign grafts. They recognize processed antigen fragments presented on MHC proteins.

  • Helper T cells (CD4): Activate B cells, other T cells, and macrophages.

  • Cytotoxic T cells (CD8): Destroy infected or abnormal cells.

  • Regulatory T cells: Help maintain tolerance.

Antigen Presentation and MHC Proteins

Antigen-presenting cells (APCs) display antigen fragments on MHC proteins to activate T cells. There are two classes of MHC proteins:

  • Class I MHC: Found on all nucleated cells; recognized by CD8 T cells.

  • Class II MHC: Found on APCs; recognized by CD4 T cells.

Immune System Disorders

Immunodeficiencies

Immunodeficiencies result from impaired production or function of immune components. Examples include congenital disorders (SCID) and acquired conditions (AIDS, Hodgkin's lymphoma).

Autoimmune Diseases

Autoimmune diseases occur when the immune system fails to distinguish self from non-self, producing autoantibodies and cytotoxic T cells that attack the body's own tissues. Examples include myasthenia gravis, multiple sclerosis, and type I diabetes mellitus.

Hypersensitivities

Hypersensitivities are exaggerated immune responses to harmless antigens (allergens). They are classified by time course and whether antibodies or T cells are involved:

  • Immediate (Type I): Allergies, mediated by IgE.

  • Subacute (Types II & III): Antibody-mediated, involve IgG and IgM.

  • Delayed (Type IV): T cell-mediated, appear in 1-3 days.

Allergic reactions may be local or systemic, with anaphylactic shock being a severe systemic response.

Summary Table: Innate vs Adaptive Defenses

Innate Defenses

Adaptive Defenses

Surface barriers (skin, mucous membranes)

Humoral immunity (B cells, antibodies)

Phagocytes, NK cells, inflammation, antimicrobial proteins, fever

Cellular immunity (T cells)

Nonspecific, always ready, no memory

Specific, systemic, memory, takes more time

Innate vs adaptive defenses table

Key Terms and Concepts

  • Pathogen: Disease-causing microorganism.

  • Antigen: Substance that provokes an immune response.

  • Opsonization: Process by which pathogens are coated to enhance phagocytosis.

  • Complement: Group of plasma proteins that aid in immune responses.

  • Immunogenicity: Ability of an antigen to provoke an immune response.

  • Self-tolerance: Ability of immune cells to avoid attacking the body's own tissues.

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