Innate and Adaptive Immune Responses to Infection

A comprehensive vocabulary review of 50 flashcards covering tissue resident cells, mechanical/chemical/microbiological intrinsic barriers, viral detection, complement activation, macrophage functions, NK cell cytotoxicity mechanisms, dendritic cell migration, and immune modules.

Tissue Resident Cells

Cells that remain positioned within tissues and perform their homeostatic functions at all times, whether an infection is present or not.

Tissue Resident Macrophage (Homeostatic Function)

A resident immune cell found in most (if not all) tissues whose homeostatic roles include clearing dead cells as well as supporting tissue growth and repair.

Tissue Resident Mast Cell (Homeostatic Function)

A resident immune cell found in most (if not all) tissues involved in homeostatic tissue remodelling and blood pressure regulation.

Innate Lymphoid Cells (ILCs) (Homeostatic Function)

Tissue resident cells present in most (if not all) tissues that maintain tissue homeostasis primarily by producing cytokines.

Tissue Resident Dendritic Cells (Homeostatic Function)

Cells resident in most (if not all) tissues that continually function to maintain immune tolerance against self.

Tissue Resident NK Cells (Homeostatic Function)

Natural killer cells resident in only some tissues that contribute to immune surveillance and growth factor production during homeostasis.

Tissue Resident Eosinophils (Homeostatic Function)

Granulocytic cells resident in only some tissues that participate in homeostatic tissue remodelling.

Mechanical Intrinsic Barriers

Physical host structures that block pathogen entry, including tight junctions between epithelial cells across all barriers, fluid/air flow, tears, and cilia.

Mucociliary Movement (Lungs)

A mechanical barrier in the respiratory tract characterized by the movement of mucus driven by epithelial cilia to sweep out foreign particles and pathogens.

Chemical Intrinsic Barriers of the Skin

Inherent cutaneous chemical defenses consisting of low pH, fatty acids, and antimicrobial peptides that restrict pathogen survival.

Pulmonary Surfactant

A chemical intrinsic barrier substance secreted in the lungs that contributes to innate biochemical defense against microbial invaders.

Chemical Intrinsic Barriers of the Eyes, Nose, and Mouth

Enzymes present in tears and saliva, alongside antimicrobial peptides, that chemically degrade or neutralize invading pathogens.

Antimicrobial Peptides

Chemical barrier molecules produced broadly across skin, gut, lung, eyes/nose/mouth, and urogenital epithelia to kill microorganisms.

Normal Microbiota

The microbiological intrinsic barrier composed of non-pathogenic commensal microorganisms residing on host epithelial surfaces that outcompete potential invaders.

RIG-I

An intracellular sensor protein inside epithelial cells that detects viral infection and triggers downstream transcription factor (TF) activation.

Interferons

Antiviral signaling cytokines produced and released by virally infected epithelial cells following transcription factor activation to alert resident immune cells.

Sentinel Macrophages

First-responding phagocytic immune cells stationed within tissues that detect and engulf viral particles entering the tissue.

Phagolysosome

The intracellular vesicle formed by the fusion of a phagosome with a lysosome, wherein digestion reveals viral nucleic acids to internal receptors.

Endosomal TLRs

Toll-like receptors located on endosomal membranes that sense viral nucleic acids unmasked within the phagolysosome.

M1-like Polarization

The pro-inflammatory phenotype induced in macrophages downstream of endosomal TLR signaling upon detecting viral pathogens.

Alternative Pathway of Complement

The complement activation cascade that is triggered spontaneously immediately upon viruses entering host tissues.

Lectin Pathway of Complement

The complement activation pathway triggered when a specific invading virus is recognized and bound by mannose-binding lectin (MBL).

Complement Opsonization

The coating of viral particles by complement fragments, which makes the virus easier for immune cells to detect via complement receptors and acts as a recruitment signal.

Membrane Attack Complex (MAC)

A multiprotein pore assembled by terminal complement components that can directly lyse and destroy enveloped virus particles.

Pro-inflammatory Macrophage Triad of Functions

Three key actions executed by activated macrophages: upregulating phagocytic/killing machinery, producing cytokines to activate other immune cells, and producing cytokines/chemokines to recruit blood cells.

Cytotoxic Module

The specialized branch of the immune response initiated during viral infection that releases molecules to recruit and activate cytotoxic cells.

Type 1 Module

The immune module coordinated against intracellular pathogens (such as viruses), working in concert with the cytotoxic module.

Chemokine Gradients

Directional chemical trails produced by tissue macrophages that circulating leukocytes follow to migrate from blood vessels to the infection site.

ILC Amplification

The process whereby local innate lymphoid cells belonging to the same immune module respond to macrophage cytokines by secreting additional cytokines to magnify the immune response.

Monocyte Recruitment (Infection)

The recruitment of circulating blood monocytes to an infected tissue, where they subsequently differentiate into macrophages and dendritic cells (DCs).

MHC-I Inhibitory Ligand

A cell surface protein expressed abundantly on healthy host cells that transmits inhibitory signals to NK cell receptors to prevent healthy cell destruction.

Stress Ligands

Surface molecules upregulated by infected or damaged host cells that engage activating NK cell receptors to tip the balance toward target cell lysis.

Viral MHC-I Downregulation

A viral evasion strategy that lowers surface MHC-I expression, which reduces NK cell inhibitory signals and inadvertently triggers NK cell mediated killing.

Granzyme-Mediated Killing

A cytotoxic mechanism where an NK cell releases perforin and granzyme; perforin facilitates granzyme entry to activate intracellular mediators of apoptosis.

Perforin

A pore-forming cytolytic protein released by NK cells that permeabilizes membranes to allow entry of granzymes into target cells.

Granzymes

Pro-apoptotic serine proteases released from NK cell granules that enter target cells and activate internal mediators of apoptosis.

FasL / Fas Death Receptor Pathway

A cytotoxic killing mechanism wherein NK cell FasL binds target cell Fas, recruiting death domain-containing proteins to trigger apoptosis mediators.

TNF-$\alpha$ Cytotoxic Pathway

A cytotoxic mechanism where NK cell TNF-$\alpha$ engages TNFR on target cells, activating death domain-containing proteins to trigger apoptotic cell death.

Apoptosis (NK-Induced)

The programmed mode of cell death induced by NK cells via granzymes, death receptors, or cytokines to eliminate infected cells without provoking excessive necrosis.

Micropinocytosis (Dendritic Cells)

The non-specific, bulk fluid uptake mechanism utilized continuously by dendritic cells in tissues to sample their local extracellular environment.

Costimulatory Molecules (DC Activation)

Molecules upregulated on the surface of dendritic cells following TLR-mediated pathogen sensing, essential for the subsequent activation of adaptive immune cells.

Draining Lymph Node

The regional lymph node that drains fluid and lymphatics from an infected tissue, serving as the anatomical site where migrating DCs activate T and B lymphocytes.

Extravasation

The multi-step process by which circulating immune cells in the bloodstream exit through the vessel wall and migrate into infected tissues.

Efferocytosis

The phagocytic clearance of apoptotic, dead, and damaged host cells or pathogen debris by tissue macrophages.

Adaptive Immune Response Induction Timeline

The $4\text{--}7\text{ days}$ post-infection interval required for dendritic cells to prime lymphocytes and for a massive, highly effective adaptive response to migrate to the tissue.

ILC1 (Type 1 Module)

Tissue resident innate lymphoid cells activated during viral infections that secrete cytokines in alignment with the cytotoxic/type 1 intracellular pathogen module.

ILC3 (Extracellular Bacterial Infection)

Innate lymphoid cells that coordinate with macrophages during extracellular bacterial infections to amplify the antibacterial immune response.

NETosis

A specialized neutrophil death pathway occurring during extracellular bacterial infection that releases neutrophil extracellular traps to ensnare and kill bacteria.

ILC2 (Parasitic Infection)

Innate lymphoid cells activated during tissue-invasive parasitic worm infections to produce cytokines supporting anti-parasitic immune defenses.

Eosinophil Degranulation (Parasitic Response)

The release of stored toxic granule proteins by tissue eosinophils directed against invasive parasitic worms and their products.