The Immune System: Innate and Adaptive Body Defenses – Microbiology Study Notes

The Immune System: Overview

Introduction to the Immune System

The immune system provides resistance to disease-causing microorganisms, including bacteria, fungi, and viruses. It is a functional system composed of various molecules and immune cells, especially lymphocytes, that reside in lymphoid tissues and circulate in body fluids. The immune system is organized into three lines of defense, which act both independently and cooperatively to resist invasion by pathogens.

• First Line of Defense: Surface barriers (skin and mucosae)

• Second Line of Defense: Innate internal defenses (e.g., phagocytes, inflammation)

• Third Line of Defense: Adaptive (specific) defense system (e.g., B and T lymphocytes)

Key Point: Innate and adaptive defenses are integrated and work together to protect the body from infectious microbes, cancer cells, and transplanted tissues.

Innate (Nonspecific) Defenses

Surface Barriers: The First Line of Defense

Surface barriers, including the skin and mucous membranes, are the body's first line of defense against pathogens. These barriers are supported by their secretions, which inhibit or destroy microbes.

• Skin: The keratinized epidermis forms a mechanical barrier; keratin is resistant to acids, bases, bacterial enzymes, and toxins.

• Mucosae: Line body tracts and provide mechanical barriers; produce protective chemicals.

• Protective Chemicals:

  • Acid Mantle: Acidity of skin, vaginal, and stomach secretions inhibits bacterial growth.

  • Enzymes: Lysozyme in saliva, mucus, and tears destroys microbes; stomach enzymes digest pathogens.

  • Mucin: Forms sticky mucus that traps microbes in digestive and respiratory tracts.

  • Defensins: Antimicrobial peptides that inhibit microbial growth.

  • Other Chemicals: Sebum lipids and dermcidin in sweat are toxic to bacteria.

• Respiratory Tract Modifications: Mucus-coated hairs trap particles; cilia sweep mucus toward the mouth.

Category/Associated Elements	Protective Mechanism
Intact skin epidermis	Mechanical barrier; prevents entry of pathogens and harmful substances
Acid mantle of skin; Keratin	Inhibits bacterial growth; resists acids, alkalis, and bacterial enzymes
Intact mucous membranes	Mechanical barrier; prevents entry of pathogens
Mucus, Nasal hairs, Cilia	Trap and filter microorganisms; propel debris-laden mucus away
Gastric juice, Acid mantle of vagina	Destroy pathogens; inhibit microbial growth
Lacrimal secretion (tears), Saliva, Urine	Cleanse and lubricate; contain lysozyme; acid pH inhibits bacterial growth

Innate Internal Defenses: The Second Line of Defense

If pathogens breach surface barriers, innate internal defenses are activated. These include phagocytes, natural killer (NK) cells, antimicrobial proteins, inflammation, and fever. Recognition of pathogens is mediated by pattern recognition receptors, such as Toll-like receptors (TLRs).

• Phagocytes: White blood cells that ingest and digest foreign invaders and debris.

  • Neutrophils: Most abundant; first responders to infection.

  • Macrophages: Derived from monocytes; free macrophages wander tissues, fixed macrophages reside in specific organs.

• Phagocytosis Process:

  1. Phagocyte binds to pathogen via receptors.

  2. Pathogen is engulfed into a phagosome.

  3. Phagosome fuses with lysosome to form phagolysosome.

  4. Lysosomal enzymes digest the pathogen.

  5. Some pathogens resist digestion; helper T cells can stimulate a respiratory burst to kill them.

• Opsonization: Pathogens are coated with opsonins (complement proteins or antibodies) to enhance phagocytosis.

• Natural Killer (NK) Cells: Large granular lymphocytes that induce apoptosis in virus-infected or cancerous cells; secrete chemicals to enhance inflammation.

Inflammation: Tissue Response to Injury

Inflammation is a nonspecific response to tissue injury, characterized by redness, heat, swelling, pain, and sometimes impaired function. It prevents the spread of pathogens, disposes of debris, alerts the adaptive immune system, and sets the stage for repair.

• Inflammatory Chemical Release: Histamine, kinins, prostaglandins, cytokines, and complement are released, causing vasodilation and increased capillary permeability.

• Phagocyte Mobilization: Four steps—leukocytosis, margination, diapedesis, and chemotaxis—bring neutrophils and monocytes to the site of injury.

• Pus and Abscess Formation: Accumulation of dead cells and pathogens may form pus; chronic infection can lead to granuloma formation.

Chemical	Source	Physiological Effects
Histamine	Mast cells, basophils	Vasodilation, increased permeability, exudate formation
Kinins	Plasma protein (kininogen)	Same as histamine; chemotaxis; pain induction
Prostaglandins	All cell membranes	Same as histamine; chemotaxis; pain induction
Complement	Plasma proteins	Amplifies inflammation, cell lysis
Cytokines	Various immune cells	Regulate immune responses

Antimicrobial Proteins

Antimicrobial proteins enhance innate defenses by attacking microbes or hindering their reproduction. The most important are interferons and complement proteins.

• Interferons (IFNs): Proteins produced by virus-infected cells; interfere with viral replication in neighboring cells and activate NK cells and macrophages.

• Complement System: A group of at least 20 plasma proteins that, when activated, amplify inflammation, promote phagocytosis (opsonization), and cause cell lysis via the membrane attack complex (MAC).

• Activation Pathways: Classical (antibody-dependent), lectin (sugar-binding proteins), and alternative (spontaneous activation on pathogen surfaces).

Fever

Fever is a systemic response to infection, mediated by pyrogens released by leukocytes and macrophages. It increases metabolic rate, enhances immune cell migration, and inhibits bacterial growth by reducing available iron.

Adaptive (Specific) Defenses

Overview of Adaptive Immunity

The adaptive immune system is a specific defense system that targets and eliminates nearly any pathogen or abnormal cell. It consists of two overlapping arms: humoral (antibody-mediated) and cellular (cell-mediated) immunity.

• Humoral Immunity: Mediated by B lymphocytes and antibodies; targets extracellular pathogens.

• Cellular Immunity: Mediated by T lymphocytes; targets infected or abnormal cells.

• Key Features: Specificity, memory, systemic response, and slower activation compared to innate defenses.

Adaptive Defenses	Innate Defenses
B and T lymphocytes; specific; slow; memory; systemic	NK cells, phagocytes, barriers; nonspecific; fast; no memory; local

Antigens

Antigens are substances that provoke an immune response. Most are large, complex molecules not normally found in the body (nonself). Antigenic determinants are specific regions of an antigen recognized by antibodies or lymphocyte receptors.

• Complete Antigens: Immunogenic and reactive; include proteins, polysaccharides, lipids, nucleic acids.

• Haptens: Incomplete antigens; small molecules that become immunogenic when attached to a carrier protein.

• Self-Antigens (MHC Proteins): Glycoproteins unique to each individual; present peptides to T cells; basis for self-tolerance and transplant rejection.

Cells of the Adaptive Immune Response

• B Lymphocytes (B cells): Provide humoral immunity; mature in bone marrow.

• T Lymphocytes (T cells): Provide cellular immunity; mature in thymus.

• Antigen-Presenting Cells (APCs): Dendritic cells, macrophages, and B cells; present antigens to T cells.

Lymphocyte Development: Originates from hematopoietic stem cells; undergoes maturation (immunocompetence and self-tolerance), seeding of secondary lymphoid organs, antigen encounter and activation (clonal selection), and proliferation/differentiation into effector and memory cells.

Humoral Immunity: Antibody-Mediated Response

B cells are activated when their receptors bind to specific antigens, leading to clonal selection. Most activated B cells become plasma cells that secrete antibodies; some become memory cells for rapid future responses.

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

• Secondary Immune Response: Subsequent exposure; faster, stronger, longer-lasting due to memory cells.

Active and Passive Humoral Immunity

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

  • Natural: Infection

  • Artificial: Vaccination

• Passive Immunity: Antibodies are acquired from another source; no memory formed.

  • Natural: Maternal antibodies (placenta, milk)

  • Artificial: Injection of antibodies (e.g., antivenom, antitoxin)

Antibodies (Immunoglobulins, Igs)

Antibodies are Y-shaped proteins produced by plasma cells. They bind specifically to antigens and are classified into five major classes: IgM, IgA, IgD, IgG, and IgE.

Class	Structure	Key Characteristics
IgM	Pentamer	First antibody released; potent agglutinating agent; activates complement
IgA	Dimer	In secretions (saliva, milk); prevents pathogen attachment to mucosa
IgD	Monomer	B cell antigen receptor
IgG	Monomer	Most abundant; crosses placenta; main antibody of secondary response
IgE	Monomer	Binds to mast cells/basophils; mediates allergic reactions and defense against parasites

• Antibody Functions: Antibodies do not destroy antigens directly but inactivate and tag them for destruction by:

  • Neutralization

  • Agglutination

  • Precipitation

  • Complement activation

• Monoclonal Antibodies: Laboratory-produced antibodies specific for a single antigenic determinant; used in diagnostics and therapy.

Cellular Immunity: T Lymphocytes

T cells provide cellular immunity by directly attacking infected or abnormal cells or by regulating other immune cells. They require antigen presentation on MHC proteins for activation.

• Major Types of T Cells:

  • Helper T (TH) Cells (CD4): Activate B cells, other T cells, and macrophages; direct immune response.

  • Cytotoxic T (TC) Cells (CD8): Destroy infected, cancerous, or foreign cells via perforins and granzymes or by inducing apoptosis.

  • Regulatory T (TReg) Cells: Suppress immune response; maintain self-tolerance.

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

• MHC Proteins:

  • Class I MHC: On all nucleated cells; present endogenous antigens to CD8 cells.

  • Class II MHC: On APCs; present exogenous antigens to CD4 cells.

• Activation of T Cells: Requires antigen binding and co-stimulation; leads to clonal selection and differentiation into effector and memory cells.

• Cytokines: Chemical messengers (e.g., interleukins, interferons) that regulate immune responses.

Cell Type	Function
B cell	Produces plasma cells and memory cells; humoral immunity
Plasma cell	Secretes antibodies
Helper T cell (TH)	Central to humoral and cellular immunity; activates B and T cells, macrophages
Cytotoxic T cell (TC)	Kills infected and cancerous cells
Regulatory T cell (TReg)	Suppresses immune response; prevents autoimmunity
Antigen-presenting cell (APC)	Engulfs and presents antigens to T cells

Immune System Disorders

Immunodeficiencies

Immunodeficiencies are conditions that impair the function or production of immune cells or molecules. They can be congenital (e.g., SCID syndromes) or acquired (e.g., AIDS, Hodgkin's lymphoma).

• SCID: Genetic defect; deficit in B and T cells; treated with stem cell transplant or gene therapy.

• AIDS: Caused by HIV; destroys helper T cells; treated with antiviral drug combinations.

Autoimmune Diseases

Autoimmunity occurs when the immune system fails to distinguish self from nonself, attacking the body's own tissues. Examples include rheumatoid arthritis, type 1 diabetes, multiple sclerosis, and lupus.

• Treatment: Immunosuppressive drugs, cytokine blockers, therapies to restore self-tolerance.

• Causes: Foreign antigens resembling self, new self-antigens from mutations or trauma, failure of self-tolerance mechanisms.

Hypersensitivities

Hypersensitivities are immune responses to harmless antigens that cause tissue damage. They are classified by time course and mechanism.

• Immediate (Type I, Allergies): IgE-mediated; rapid onset; histamine release causes allergy symptoms; severe cases may cause anaphylactic shock.

• Subacute (Type II, Cytotoxic; Type III, Immune Complex): IgM/IgG-mediated; slower onset; involve complement activation and inflammation.

• Delayed (Type IV): T cell-mediated; appear 1–3 days after exposure; involve macrophage activation and tissue damage (e.g., contact dermatitis, TB skin test).

Developmental Aspects and Aging of the Immune System

• Immune system stem cells develop in liver and spleen in early fetal life; bone marrow becomes primary source later.

• Newborns rely on maternal antibodies and TH2 lymphocytes; exposure to microbes strengthens TH1 responses.

• With age, immune efficiency declines, increasing susceptibility to infections, cancer, and autoimmune diseases.

• Thymus atrophies after puberty, reducing naive T and B cell production.

• Chronic low-grade inflammation in older adults may contribute to age-related diseases.

Additional info: This summary integrates core concepts from immunology relevant to microbiology, including the mechanisms of innate and adaptive immunity, the roles of various immune cells and molecules, and clinical implications such as immunodeficiencies, autoimmunity, and hypersensitivity reactions.