BackChapter 21: The Immune System – Innate and Adaptive Body Defenses
Study Guide - Smart Notes
Tailored notes based on your materials, expanded with key definitions, examples, and context.
The Immune System
The immune system is a complex network of cells, tissues, and molecules that protects the body from pathogens and abnormal cells. It is divided into innate (nonspecific) and adaptive (specific) defenses, each with distinct mechanisms and components.
Overview of Innate and Adaptive Defenses
Innate Defenses: Present at birth, these defenses provide immediate, nonspecific protection against pathogens.
Adaptive Defenses: Develop after exposure to antigens and provide specific, long-lasting protection.
First, Second, and Third Lines of Defense
First Line (Surface Barriers):
Physical barriers: Skin and mucous membranes
Chemical barriers: Acid mantle of skin, enzymes (e.g., lysozyme in saliva, tears), defensins (antimicrobial peptides)
Defensin: Small proteins that disrupt microbial membranes.
Lysozyme: Enzyme that breaks down bacterial cell walls.
Second Line (Internal Defenses):
Cells: Phagocytes (neutrophils, macrophages), natural killer (NK) cells
Chemicals: Interferons, complement proteins
Processes: Inflammation, fever
Respiratory burst: Rapid release of reactive oxygen species by phagocytes to destroy pathogens.
Third Line (Adaptive Defenses):
Humoral immunity: Mediated by B cells and antibodies
Cellular immunity: Mediated by T cells
Inflammation
Inflammation is a localized response to injury or infection, designed to eliminate the initial cause of cell injury, clear out damaged cells, and establish repair.
Steps of Inflammation:
Release of inflammatory chemicals (e.g., histamine, prostaglandins)
Vasodilation and increased vascular permeability
Phagocyte mobilization (neutrophils, then macrophages)
Tissue repair
Interferon
Interferons are proteins released by virus-infected cells that help protect uninfected cells by stimulating antiviral protein production.
Complement Activation
The complement system is a group of plasma proteins that enhance immune responses.
Opsonization: The process by which complement proteins coat pathogens, enhancing phagocytosis.
Three Pathways:
Classical pathway: Triggered by antibodies bound to antigens.
Lectin pathway: Triggered by lectins binding to microbial carbohydrates.
Alternative pathway: Triggered directly by pathogen surfaces.
Fever
Fever is an abnormally high body temperature that enhances immune function and inhibits pathogen growth.
Adaptive Defenses
Adaptive immunity involves specific recognition of antigens and memory formation. It is divided into humoral and cellular immunity.
Humoral Immunity: B cells produce antibodies that circulate in body fluids.
Cellular Immunity: T cells directly attack infected or abnormal cells.
Antigens
Antigen: Any substance that can provoke an immune response.
Complete Antigen: Has both immunogenicity (can stimulate lymphocytes) and reactivity (can react with lymphocytes/antibodies). Examples: proteins, polysaccharides.
Incomplete Antigen (Hapten): Reactive but not immunogenic unless attached to a carrier. Examples: small molecules like penicillin.
MHC Proteins
MHC Class I: Found on all nucleated cells; present endogenous antigens to CD8+ cytotoxic T cells.
MHC Class II: Found on antigen-presenting cells (APCs) like dendritic cells, macrophages, B cells; present exogenous antigens to CD4+ helper T cells.
Lymphocytes and Antigen-Presenting Cells (APCs)
APCs: Dendritic cells, macrophages, and B cells. They process and present antigens to T cells via MHC molecules.
Lymphocyte Development, Maturation, and Activation
Origin: All lymphocytes originate in red bone marrow.
Maturation: B cells mature in bone marrow; T cells mature in thymus.
Activation: Occurs when lymphocytes encounter their specific antigen.
T Cell Education in the Thymus
Positive Selection: T cells must recognize self-MHC molecules to survive.
Negative Selection: T cells that bind too strongly to self-antigens are eliminated (prevents autoimmunity).
Clonal Selection
B Cells: Upon activation, B cells proliferate and differentiate into plasma cells (antibody producers) and memory B cells.
T Cells: Upon activation, T cells proliferate and differentiate into effector and memory T cells.
Antibody Structure
Antibodies have variable regions that bind specific antigens and constant regions that determine class and function.
Antibodies responding to different antigens have different variable regions.
Immunoglobulin Classes
IgM: First antibody produced in response to infection; pentamer structure.
IgG: Most abundant; provides long-term immunity; crosses placenta.
IgA: Found in mucosal areas and secretions (saliva, tears).
IgE: Involved in allergic reactions and defense against parasites.
IgD: Functions mainly as a B cell receptor.
Mechanism of Antibody Action
Neutralization: Antibodies block pathogen binding sites.
Agglutination: Antibodies cause pathogens to clump together.
Precipitation: Antibodies cause soluble antigens to become insoluble and precipitate.
Complement Activation: Antibodies trigger the complement cascade, leading to cell lysis.
Effects: Enhanced phagocytosis, inflammation, and cell lysis.
Major Types of T Cells
Helper T Cells (CD4+): Activate B cells, cytotoxic T cells, and macrophages; coordinate immune response.
Cytotoxic T Cells (CD8+): Destroy infected and cancerous cells.
Regulatory T Cells: Suppress immune responses to prevent autoimmunity.
Helper T Cells Mobilizing Both Humoral and Cellular Immunity
Helper T cells release cytokines that stimulate B cells (humoral) and cytotoxic T cells (cellular).
Cytotoxic T Cells Attack Infected and Cancerous Cells
Cytotoxic T cells induce apoptosis in target cells via perforin and granzymes.
Difference from NK Cells: Cytotoxic T cells require antigen presentation via MHC I; NK cells do not.
Primary vs. Secondary Humoral Responses
Primary Response: First exposure to antigen; slower; mainly IgM produced.
Secondary Response: Subsequent exposures; faster and stronger; mainly IgG produced.
Active vs. Passive Humoral Immunity
Active Immunity: Body produces its own antibodies.
Naturally acquired: Infection
Artificially acquired: Vaccination
Passive Immunity: Antibodies are received from another source.
Naturally acquired: Maternal antibodies via placenta or breast milk
Artificially acquired: Injection of antibodies (e.g., antivenom)
Organ Transplants and Rejection
Transplanted organs may be rejected if recipient's immune system recognizes donor antigens as foreign.
Immunosuppressive drugs are used to reduce rejection risk.
Immune System Homeostatic Imbalances
Immunodeficiency: Impaired immune function. Example: Severe Combined Immunodeficiency (SCID).
Hypersensitivities
Type I (Immediate): Allergy, anaphylactic shock (IgE-mediated)
Type II (Cytotoxic): Blood transfusion mismatch (antibody-mediated)
Type III (Immune Complex): Glomerulonephritis of SLE (immune complex deposition)
Type IV (Delayed): Contact dermatitis (T cell-mediated)
Hypersensitivity Type | Example | Mechanism |
|---|---|---|
Type I (Immediate) | Allergy, anaphylactic shock | IgE-mediated, mast cell degranulation |
Type II (Cytotoxic) | Blood transfusion mismatch | IgG/IgM antibodies bind to cell surface antigens |
Type III (Immune Complex) | Glomerulonephritis of SLE | Immune complex deposition in tissues |
Type IV (Delayed) | Contact dermatitis | T cell-mediated response |
Additional info: This summary expands on the outline by providing definitions, mechanisms, and examples for each major concept, ensuring a comprehensive review for exam preparation.