Chapter 21 — The Immune System: Innate & Adaptive Defenses

A comprehensive set of vocabulary flashcards covering the key terms, cells, molecules, and mechanisms discussed in Chapter 21 (Innate and Adaptive Body Defenses) to aid exam preparation.

Immune System

Functional system of molecules and cells that provides resistance (immunity) to disease-causing microbes.

Innate (Nonspecific) Defenses

Inborn, fast defenses that guard against any invader; include surface barriers and internal cellular/chemical defenses.

Adaptive (Specific) Defenses

Slower, learned defenses that target identified antigens through B and T lymphocytes; possess memory.

Surface Barriers

First line of defense: intact skin and mucous membranes plus their secretions.

Keratin

Tough skin protein that resists weak acids, bases, enzymes, and toxins.

Acid Mantle

Acidic film of skin, vagina, and stomach secretions that inhibits bacterial growth.

Lysozyme

Enzyme in saliva, tears, and mucus that destroys bacterial cell walls.

Mucin

Protein that forms sticky mucus to trap microbes in respiratory and digestive tracts.

Defensins

Broad-spectrum antimicrobial peptides released by skin and mucosae when breached.

Pattern-Recognition Receptors (PRRs)

Innate cell receptors that bind shared molecular shapes on microbes.

Toll-Like Receptors (TLRs)

Key PRRs (11 types) that trigger innate immune responses upon binding microbes.

Phagocytes

White blood cells that ingest and digest pathogens and debris.

Neutrophils

Most abundant phagocytes; first responders that engulf and die fighting infection.

Macrophages

Highly voracious phagocytes derived from monocytes (free or fixed in tissues).

Phagolysosome

Vesicle formed by fusion of a phagosome with a lysosome where digestion occurs.

Respiratory Burst

Macrophage process generating free radicals and oxidizers to kill tough pathogens.

Opsonins

Complement proteins or antibodies that coat pathogens and enhance phagocytosis.

Opsonization

Process of tagging a pathogen with opsonins for easier phagocyte binding.

Netosis

Neutrophil death that releases DNA webs to trap and kill extracellular microbes.

Natural Killer (NK) Cells

Large granular lymphocytes that induce apoptosis in virus-infected or cancer cells without specific antigen recognition.

Apoptosis

Programmed cell death initiated by NK or cytotoxic T cells to eliminate targets.

Inflammation

Nonspecific tissue response to injury characterized by redness, heat, swelling, pain.

Histamine

Mast-cell chemical that dilates arterioles and increases capillary permeability.

Kinins

Plasma peptides that promote vasodilation, chemotaxis, and pain during inflammation.

Prostaglandins

Fatty-acid mediators that enhance inflammation and pain; blocked by aspirin.

Complement (Inflammatory)

Plasma protein cascade that amplifies inflammation and attracts phagocytes.

Hyperemia

Increased local blood flow producing heat and redness in inflamed tissue.

Exudate

Protein-rich fluid that leaks into tissues causing swelling (edema).

Leukocytosis

Rapid increase of white blood cells in bloodstream during inflammation.

Margination

Process of leukocytes sticking to capillary walls at an inflamed area.

Diapedesis

Leukocytes flattening and squeezing through capillary walls into tissues.

Chemotaxis

Chemical attraction guiding leukocytes toward site of injury or infection.

Pus

Creamy mixture of dead neutrophils, tissue cells, and microbes.

Abscess

Walled-off pocket of pus requiring drainage for healing.

Granuloma

Tumor-like mass of infected macrophages surrounded by fibrous capsule (e.g., TB).

Interferons (IFNs)

Antiviral cytokines that block viral replication and activate NK cells & macrophages.

Complement System

~20 plasma proteins that, when activated, enhance inflammation, opsonize, or lyse cells.

Membrane Attack Complex (MAC)

Complement-formed pore that allows water influx and lyses target cells.

Pyrogens

Leukocyte-secreted chemicals that reset hypothalamic thermostat, producing fever.

Fever

Systemic rise in body temperature that accelerates repair and inhibits microbes.

Antigen

Substance that provokes an adaptive immune response (antibody-generating).

Complete Antigen

Molecule with immunogenicity and reactivity that can activate lymphocytes itself.

Hapten

Small molecule that becomes antigenic only when attached to a body protein.

Antigenic Determinant

Specific part of antigen that antibodies or receptors bind; one antigen has many.

Major Histocompatibility Complex (MHC) Proteins

Self glycoproteins that display peptide fragments to T cells.

B Lymphocytes (B Cells)

Lymphocytes that mature in bone marrow and mediate humoral immunity.

T Lymphocytes (T Cells)

Lymphocytes that mature in thymus and provide cellular immunity.

Antigen-Presenting Cells (APCs)

Cells (dendritic, macrophages, B cells) that display antigen fragments to T cells.

Dendritic Cells

Mobile APCs in skin/mucosa that capture antigens and migrate to lymph nodes.

Clonal Selection

Activation and proliferation of a lymphocyte clone after it binds its specific antigen.

Plasma Cells

Effector B cells that secrete large volumes of antibodies.

Memory Cells

Long-lived B or T cells that respond rapidly on future exposure to the same antigen.

Primary Immune Response

First adaptive response; slow (3–6 day lag) with IgM then IgG production.

Secondary Immune Response

Subsequent exposure producing faster, stronger, longer-lasting antibody titers.

Active Humoral Immunity

Immunity developed when B cells meet antigen and make antibodies (infection or vaccine).

Passive Humoral Immunity

Short-term protection from receiving ready-made antibodies (placenta, antisera).

Immunoglobulins (Antibodies)

Gamma-globulin proteins produced by plasma cells; five classes (IgG, IgA, IgM, IgE, IgD).

IgG

Most abundant plasma antibody; crosses placenta; main secondary responder; activates complement.

IgA

Dimer antibody in secretions (saliva, milk) that blocks pathogen entry on mucosae.

IgM

Pentamer; first antibody released; strong agglutinator; useful indicator of current infection.

IgE

Antibody that binds mast cells/basophils; triggers histamine release; rises in allergies & parasites.

IgD

Surface receptor antibody on naive B cells; function in activation.

Neutralization

Antibodies block pathogen or toxin binding sites, rendering them harmless.

Agglutination

Antibodies cross-link cell-bound antigens causing clumping for easier clearance.

Precipitation

Antibodies cross-link soluble antigens into insoluble complexes for phagocytosis.

Cytotoxic T (CD8) Cells

Effector T cells that directly kill infected, cancer, or foreign cells via perforin/granzymes.

Helper T (CD4) Cells

Central coordinators that activate B cells, other T cells, and macrophages via cytokines.

Regulatory T Cells

Subset that dampens immune responses and maintains self-tolerance.

CD4 Protein

Glycoprotein co-receptor on helper T cells that binds MHC II during antigen recognition.

CD8 Protein

Co-receptor on cytotoxic T cells that binds MHC I on target cells.

Cytokines

Chemical messengers (e.g., interferons, interleukins) that regulate immunity.

Interleukin-2 (IL-2)

Key T-cell growth factor promoting rapid cell division and activation.

Interleukin-17 (IL-17)

TH17-derived cytokine linking innate and adaptive immunity; drives inflammation.

Perforin

Protein released by cytotoxic T and NK cells that forms pores in target membranes.

Granzyme

Enzyme entering target cells through perforin pores to trigger apoptosis.

Immune Surveillance

Continuous monitoring by NK and cytotoxic T cells for abnormal antigens on cells.

Immunodeficiency

Any condition (congenital or acquired) impairing immune cell or molecule function.

Severe Combined Immunodeficiency (SCID)

Genetic disorder with absent B and T cells; requires stem-cell transplant.

Acquired Immunodeficiency Syndrome (AIDS)

HIV-induced loss of CD4 cells leading to severe immune suppression.

Autoimmune Disease

Condition where self-tolerance fails and immune system attacks own tissues.

Hypersensitivity

Overactive immune responses to harmless antigens that cause tissue damage.

Anaphylactic Shock

Severe, systemic IgE-mediated allergic reaction with widespread vasodilation and airway constriction.

Cytotoxic Hypersensitivity

IgG/IgM-mediated reaction against cell-bound antigens (e.g., transfusion mismatch).

Delayed Hypersensitivity

T-cell-mediated reaction developing 1–3 days after exposure (e.g., poison ivy rash).