Chapter 11 Innate Immunity Study Guide

A set of 100 comprehensive vocabulary flashcards covering Chapter 11 Innate Immunity, including first-line physical, mechanical, and chemical barriers; the lymphatic system; cellular and molecular second-line defenses; the complement system; inflammation; and fever.

Self-Tolerance

The immune system’s ability to recognize the body’s own cells and molecules as self and avoid attacking them.

Immune Person

An individual with defenses that prevent infection or disease from a pathogen, often resulting from prior infection or vaccination.

Susceptible Person

An individual who lacks sufficient protective immunity and is more likely to become infected or ill after exposure to a pathogen.

Innate Immunity

Immune defenses present from birth that respond rapidly to threats by recognizing broad molecular patterns shared by groups of microbes, generally lacking antigen-specific memory.

Adaptive Immunity

Immune defenses that develop after exposure to a pathogen, responding more slowly on first exposure, recognizing specific antigens, and forming long-lasting memory.

Similarities of Innate and Adaptive Immunity

Both protect the body from pathogens, utilize cells and soluble molecules to detect or respond to threats, and communicate and work together to eliminate infection and limit damage.

Broad Molecular Patterns

Conserved structures shared across groups of microbes that are recognized by innate immune defenses rather than by antigen-specific receptors.

Specific Antigens

Distinct, highly specific molecular structures uniquely recognized by adaptive immune defenses.

Normal Microbiota in Immunity

Indigenous microorganisms that help train and regulate immune defenses, support lymphoid tissue development, and compete with pathogens for space and nutrients.

Hygiene Hypothesis

The hypothesis proposing that reduced exposure to diverse microbes early in life may interfere with normal immune-system development and increase the risk of allergies or some autoimmune conditions.

Primary Goal of First-Line Defenses

To prevent pathogens from entering the body or becoming established on its surfaces.

Skin (Physical Barrier)

The main first-line defense physical barrier in animals, characterized by tightly packed, continually shed cells and few openings compared with mucosal surfaces.

Epidermis

A tightly packed, multilayered sheet of epithelial cells whose outer cells are keratinized and continually shed, making microbial penetration difficult and removing attached microbes.

Mechanical Barriers

First-line defenses that physically rinse, flush, or sweep microbes and debris away from body surfaces.

Rinsing Action of Tears

A mechanical barrier that continuously washes microbes and foreign particles away from the surface of the eyes.

Flushing Action of Urine

A mechanical barrier that cleanses the urinary tract by physically expelling microbes during urination.

Mucociliary Escalator

A mechanical respiratory defense where mucus traps inhaled microbes and particles, and cilia sweep the mucus toward the throat to be swallowed or expelled.

Chemical Barriers

Substances produced by the host—such as stomach acid, lysozyme, and antimicrobial peptides—that destroy or inhibit microbes through chemical actions.

Stomach Acid

A potent chemical barrier whose low pH destroys swallowed microorganisms, preventing them from establishing in the gastrointestinal tract.

Lysozyme

A chemical enzyme present in tears, mucus, saliva, and breast milk that breaks bonds in bacterial cell wall peptidoglycan, causing susceptible bacteria to lyse.

Peptidoglycan

A structural component of bacterial cell walls that is targeted and broken down by the enzyme lysozyme.

Antimicrobial Peptides (AMPs)

Chemical defense peptides that inhibit or kill microbes, often by disrupting their cell membranes, helping protect skin and mucosal surfaces.

Defensins

Small antimicrobial peptides produced by epithelial cells and some immune cells that damage microbial membranes and help signal or recruit immune cells.

Earwax (Cerumen)

A barrier that acts mainly mechanically by trapping foreign particles, while also containing chemical substances that help inhibit microbes.

Lymphatic System

A network of vessels, tissues, and organs that collects excess fluid from tissues, returns it to the bloodstream, transports immune cells and antigens, and provides sites to organize immune responses.

Plasma

The liquid portion of blood in which blood cells, proteins, nutrients, hormones, and other dissolved substances are suspended.

Edema

Swelling caused by excess fluid accumulating in tissues.

Lymph

Interstitial fluid that has entered lymphatic vessels, transporting fluid, immune cells, and collected tissue material before returning to the bloodstream.

Primary Lymphoid Tissues

Sites where leukocytes are generated and mature, specifically the bone marrow and the thymus.

Secondary Lymphoid Tissues

Sites where immune cells encounter antigens and initiate adaptive responses, including lymph nodes, spleen, and MALT.

Bone Marrow (Lymphoid Function)

A primary lymphoid tissue where all blood cell precursors are produced and where B cells mature.

Thymus

A primary lymphoid organ located in the chest where T-cell precursors mature into functional T cells.

T-Cell Development

The process whereby T-cell precursors are produced in the bone marrow and travel to the thymus to undergo maturation.

B-Cell Development

The process whereby B-cell precursors are both produced and mature entirely within the bone marrow.

Lymph Nodes

Secondary lymphoid organs that filter lymph and bring antigens into contact with lymphocytes and other immune cells to detect pathogens and initiate adaptive responses.

Swollen Lymph Nodes (Cause)

Enlargement and tenderness resulting from immune cells multiplying and activating in response to an infection, along with increased fluid in the node.

Spleen

A secondary lymphoid organ that filters blood, removes old or damaged blood cells, detects blood-borne pathogens, and helps mount immune responses against them.

Mucosa-Associated Lymphoid Tissue (MALT)

Organized secondary mucosal lymphoid tissues that monitor mucosal surfaces; examples include tonsils, adenoids, Peyer's patches, and the appendix.

Gut-Associated Lymphoid Tissue (GALT)

Secondary mucosal lymphoid tissue associated specifically with the gastrointestinal tract.

Peyer’s Patches

Secondary lymphoid nodules located in the lining of the small intestine, especially within the ileum, functioning as part of GALT and MALT.

Granulocytes

Leukocytes characterized by prominent cytoplasmic granules, consisting of neutrophils, eosinophils, basophils, and mast cells.

Agranulocytes

Leukocytes that lack prominent cytoplasmic granules, consisting of monocytes, lymphocytes, and dendritic cells.

Differential White Blood Cell Count

A diagnostic test reporting the proportions or numbers of different white blood cell types to indicate patterns associated with infection, inflammation, or allergy.

Leukocytosis

An abnormally high white blood cell count, often occurring in response to infection or inflammation.

Neutrophils

The most abundant leukocytes in human blood and typically the first granulocytes recruited in large numbers to sites of acute injury or infection.

Neutrophil Granules

Granules containing antimicrobial substances, including lysozyme, defensins, digestive enzymes, and proteins that bind iron.

Neutropenia

An abnormally low neutrophil count that increases the risk of serious bacterial and fungal infections.

Eosinophils

Granulocytes whose granules stain red to orange with eosin dyes; counts often rise during parasitic worm infections and allergic conditions such as asthma.

Basophils

Circulating granulocytes whose granules stain dark blue to purple and contain histamine, which promotes inflammation and allergic responses.

Histamine

A notable vasoactive molecule stored in basophil and mast cell granules that promotes inflammation, vasodilation, and allergic responses.

Mast Cells

The main tissue-resident granulocytes that produce and release histamine to induce vascular changes during inflammation.

Monocytes

Circulating agranulocytes that enter tissues and commonly differentiate into macrophages or dendritic cells.

Macrophages

Major phagocytic cells in tissues derived from extravasated monocytes that engulf pathogens and dead cells.

Dendritic Cells

Agranulocytes abundant at barrier tissues like skin and mucosal surfaces that capture antigens and help activate adaptive immunity.

Key Phagocytic Agranulocytes

Monocytes and dendritic cells, as well as monocyte-derived macrophages.

Natural Killer (NK) Cells

Lymphocytes primarily involved in innate immunity that destroy virus-infected or abnormal cells.

B Cells and T Cells

Lymphocytes that mediate adaptive immunity, recognizing specific antigens and forming long-term immunological memory.

Cytokines

Small signaling proteins released by cells that influence the behavior, activity, movement, growth, or survival of other cells, especially immune cells.

Cytokine Storm

An excessive, poorly controlled release of inflammatory cytokines that can cause widespread inflammation, tissue damage, shock, and potentially organ failure.

Chemokines

Cytokines that attract immune cells and guide their movement toward sites of infection or tissue damage.

Chemotaxis

Directed cell movement along a chemical gradient, such as immune cells moving toward a higher concentration of signals at an infection site.

Interleukins

Signaling molecules that help immune cells communicate and regulate immune-cell activation, growth, differentiation, and coordination of responses.

Apoptosis

A regulated form of programmed cell death that allows the body to remove unwanted, damaged, or infected cells while limiting inflammation.

Tumor Necrosis Factor Alpha (TNF-α)

An inflammatory cytokine primarily made by activated macrophages that promotes inflammation, activates blood-vessel lining cells, recruits immune cells, and contributes to fever.

Siderophores

Microbial molecules that bind iron very tightly to help microbes capture and import iron, which is scarce in the host because host proteins bind it.

Transferrin and Lactoferrin

Host iron-binding proteins that tightly sequester iron, preventing microbes from easily obtaining it for growth.

Microbial Mechanisms of Iron Acquisition

Four strategies used by microbes: releasing siderophores, using surface receptors to capture iron from transferrin/lactoferrin, acquiring heme/hemoglobin via receptors, and producing hemolysins.

Hemolysins

Microbial factors that damage red blood cells or tissues to release hemoglobin and heme for microbial iron scavenging.

Heme-Binding Proteins

Microbial surface receptors and proteins that capture iron directly from host heme or hemoglobin.

Complement System

A molecular second-line defense system consisting of circulating proteins that destroy microbes via opsonization, inflammation, and membrane lysis.

Complement Component C3

The central complement component where the classical, lectin, and alternative activation pathways converge.

Complement Fragment C3a

A small complement fragment produced by the cleavage of C3 that promotes inflammation and immune-cell recruitment.

Complement Fragment C3b

A cleavage fragment of C3 that coats microbes for opsonization and helps form enzyme complexes that drive later complement steps.

Classical Pathway

A complement pathway activated mainly when antibodies bound to a microbial target recruit complement proteins.

Lectin Pathway

A complement pathway that begins when mannose-binding lectin or related recognition proteins bind microbial carbohydrates.

Alternative Pathway

A complement pathway that begins through low-level spontaneous C3 activation that is amplified on microbial surfaces lacking protective host regulators.

Outcomes of Complement Activation

Three outcomes: inflammation and immune-cell recruitment (via C3a/C5a), opsonization (via C3b), and direct cell lysis by the membrane attack complex.

Opsonization

The coating of a pathogen with molecules such as C3b or antibodies that make it easier for phagocytes to recognize and engulf.

Membrane Attack Complex (MAC)

A pore-forming assembly of complement proteins that inserts into a target membrane and can cause cell lysis.

Regulators of Complement Activation (RCAs)

Host proteins that control complement activity, limit amplification, and protect self-cells from damage; some microbes produce or capture similar proteins to evade complement.

Goals of Inflammation

To eliminate or neutralize the cause of injury or infection, contain it to limit spread, and begin removal of damaged tissue and repair.

Cardinal Signs of Inflammation

Redness, heat, swelling, and pain; reduced function can also occur.

Vascular Changes Phase of Inflammation

The initial inflammatory stage where local blood vessels dilate and become more permeable, increasing blood flow and allowing fluid and proteins to enter tissue.

Leukocyte Recruitment and Clearance Phase

The inflammatory stage where immune cells leave the blood, migrate to the injury site, and remove microbes and debris.

Resolution and Repair Phase

The final inflammatory stage where inflammation subsides, damaged material is cleared, and tissue healing begins.

Vasodilation

Widening of blood vessels due to relaxation of smooth muscle in their walls, which increases blood flow to the affected area.

Vasoactive Molecules in Inflammation

Mediators such as histamine, eicosanoids, and kinins that induce vascular changes; mast cells are the main tissue-resident producers, while basophils also release them.

Antihistamines

Medications that reduce histamine’s effects, commonly by blocking histamine receptors, lessening symptoms such as itching, swelling, and mucus production.

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

Drugs that inhibit cyclooxygenase (COX) enzymes, reducing the production of pain- and inflammation-promoting prostaglandins and related eicosanoids.

Steroidal Anti-Inflammatory Drugs (SAIDs)

Anti-inflammatory drugs such as glucocorticoids that act broadly by reducing inflammatory gene expression and the production of multiple inflammatory mediators.

Margination

The movement of leukocytes toward and along the inner surface of the blood-vessel wall, where they slow down and adhere.

Diapedesis (Transmigration)

The passage of adhered leukocytes between endothelial cells through the vessel wall into surrounding tissue.

First Leukocyte Responders to Damaged Tissue

Neutrophils arrive first in large numbers, followed by monocytes that differentiate into macrophages within the tissue.

Angiogenesis

The formation of new blood vessels from existing vessels, which helps supply oxygen and nutrients during tissue repair.

Specialized Pro-Resolving Lipid Mediators (SPMs)

Signaling lipids made from fatty acids (including resolvins, protectins, maresins, and lipoxins) that help bring inflammation to an orderly resolution.

Functions of SPMs

Stopping further recruitment of inflammatory cells, promoting phagocytic clearance of microbes and dead cells, and supporting tissue repair and return to normal function.

Long-Term Advantage of SPMs over NSAIDs

SPMs promote active resolution of inflammation rather than broadly blocking pathways, potentially preserving protective functions and avoiding risks of chronic NSAID use.

Pyrogens

Substances that cause fever by signaling the hypothalamus to raise the body’s temperature set point, prompting heat production (e.g., shivering) and conservation.

Antipyretic Drugs

Drugs, such as acetaminophen and NSAIDs, that lower fever by reducing prostaglandin signaling in the hypothalamus to return the temperature set point toward normal.

Fevers of $105^\circ\text{F}$ or Above

Life-threatening body temperatures at which enzymes and proteins lose function and cells are damaged, increasing the risk of neurologic injury, seizures, dehydration, and organ failure.