Immunology: Innate and Historical Foundations

Vocabulary flashcards covering core immunology principles, historical milestones, complement cascades, innate immune receptors, and cellular mechanisms.

Clusters of Differentiation (CD)

A standardized nomenclature system established to classify cell surface proteins, encompassing over 370 markers across diverse immune cells to prevent confusion from multiple names.

Pathogen Attenuation

A technique discovered by Louis Pasteur where heat weakens pathogens without killing them, allowing their use in vaccines such as those for anthrax and rabies.

Germ Theory of Disease

The scientific principle demonstrating that infectious diseases are caused by microorganisms (such as bacteria and viruses), establishing that specific immune responses can be generated against them through vaccination.

Innate Immune System

The first line of defense present at most tissue sites that recognizes broad classes of pathogens using both cellular components (such as macrophages and neutrophils) and humoral factors (such as complement).

Macrophages

Innate immune phagocytes derived from blood monocytes that engulf pathogens and present antigens to initiate immune responses.

T Cells

Adaptive immune cells capable of distinguishing between specific strains of a pathogen and generating highly specific responses.

Phagocytes

Specialized immune cells that primarily perform phagocytosis to engulf pathogens, which include macrophages, dendritic cells, and B cells.

C3 Cleavage

The central driving step of complement activation where all three pathways converge to cleave C3 into fragments C3a and C3b.

Alternative Pathway

The fastest-acting complement pathway that can activate immediately on pathogen surfaces in the absence of antibodies.

Classical Pathway

The slowest complement pathway during initial pathogen exposure that utilizes antibodies to direct targets for C3b-mediated phagocytosis, activating faster upon re-exposure.

Mannose-Binding Lectin (MBL)

A pattern recognition receptor (PRR) that binds to carbohydrates on pathogen surfaces to initiate the lectin complement cascade.

Damage-Associated Molecular Pattern (DAMP)

An endogenous host-derived molecular indicator of cell damage or metabolic stress, such as a drop in local pH, recognized by innate receptors.

Natural Killer (NK) Cells

Innate lymphocytes derived from the common lymphoid progenitor that eliminate virally infected cells and tumor cells by releasing cytotoxic granules containing perforin and granzymes.

Microbiota

Commensal microorganisms inhabiting mucosal barriers that occupy surface area to physically prevent opportunistic pathogens from attaching and establishing infection.

Trained Immunity

An innate immune adaptation where cells such as monocytes and NK cells undergo epigenetic and chromatin modifications after a primary encounter, enabling a faster and more intense, non-specific response upon subsequent exposures.

Neutrophils

Highly abundant circulating microphages that serve as the fastest-recruited first responders to an infection site, utilizing PRRs to generate broad responses that can cause host tissue collateral damage.

Dendritic Cells

Sentinel innate immune cells that detect pathogens via pattern recognition receptors (PRRs) and release cytokines to coordinate and modulate the activity of other immune cells.

Kupffer Cells

Tissue-resident macrophages specialized within the liver to filter circulating blood and remove toxins.

Microglia

Tissue-resident macrophages specialized within the brain to maintain neural homeostasis and respond to neuronal injury.

Variolation

An early method of smallpox immunization involving the direct transfer of infectious matter from smallpox lesions, bearing a substantial risk of severe illness and death.

Cross-Protection

An immunological concept demonstrated by Edward Jenner's smallpox vaccine, wherein exposure to a related, less virulent pathogen (cowpox) establishes protective immunity against a severe disease.

Killer Inhibitory Receptors (KIRs)

Surface receptors on NK cells that bind self-MHC class I molecules to deliver an inhibitory signal that suppresses cytotoxicity.

Killer Activation Receptors (KARs)

Surface receptors on NK cells that recognize stress-induced ligands on target cells, stimulating cytotoxic killing when inhibitory KIR signals are absent or diminished.

Cytokine Storm

A state of hyperinflammation caused by uncontrolled cytokine release during severe infection, leading to widespread collateral tissue damage, debilitating pain, and organ dysfunction.

Phagolysosome Inhibition

A pathogenic survival mechanism employed by organisms like Mycobacterium tuberculosis that prevents phagosome-lysosome fusion, allowing replication inside macrophage endosomes.

Toll-Like Receptor 3 (TLR-3)

An intracellular pattern recognition receptor that recognizes viral double-stranded RNA to trigger antiviral innate responses.

Toll-Like Receptor 5 (TLR-5)

A pattern recognition receptor that detects bacterial flagellin, the molecular motor component of flagellated bacteria.

Local Vasodilation

A vascular response in local inflammation that widens blood vessel diameter, decreases blood flow velocity, and increases vessel permeability to assist immune cells in emigrating into infected tissue.

Eosinophils

Granulocytic white blood cells that primarily degranulate to release cytotoxic contents aimed at controlling large multicellular organisms.

Type I Interferons

Cytokines that, when present prior to infection, prime the immune system by upregulating interferon-stimulated genes to enhance viral clearance and prevent cytokine storms.

NETosis

A form of neutrophil activation and death that expels webs of extracellular DNA into the bloodstream to capture and neutralize pathogens.