Immunology: Intrinsic Barriers and Innate Sensing

Vocabulary practice flashcards covering intrinsic immune barriers, microbial defenses, complement pathways, pattern recognition receptors, and danger sensing.

Microbial Dysbiosis

An improper composition or reduced diversity of bacteria in the microbiome that predisposes the host to infection and weakens barrier function.

Zymogens

Inactive precursor proteins, such as complement protein $C3$, that require enzymatic cleavage into active fragments like $C3a$ and $C3b$ to execute immunological functions.

Cathelicidins

A class of antimicrobial peptides continuously expressed by epithelial cells at barrier surfaces, represented in humans exclusively by $LL\text{-}37$.

Membrane Attack Complex (MAC)

A pore-forming complex generated at the end of the complement cascade that disrupts pathogen cell membranes and causes cell lysis.

Alternative Pathway

The first complement pathway to be activated, initiated when complement proteins spontaneously cleave directly on the surface of a pathogen.

Lectin Pathway

The second complement pathway to be activated, initiated when Mannose-binding lectin (MBL) detects non-self glycans on pathogen surfaces.

Classical Pathway

The final complement pathway to be activated, triggered when antibodies generated by the adaptive immune system bind to pathogen antigens.

Self / Non-Self Discrimination Hypothesis

The immunological model proposed by Frank Macfarlane Burnet stating that the immune system recognizes self-antigens to maintain tolerance while attacking foreign non-self targets.

Pathogen Associated Molecular Patterns (PAMPs)

Evolutionarily conserved molecular structures essential for microbial survival—such as peptidoglycan or LPS—that are detected by host pattern recognition receptors.

Danger Hypothesis

The immune paradigm formulated by Polly Matzinger proposing that the immune system senses markers of cellular distress and tissue injury rather than non-self alone.

Damage Associated Molecular Patterns (DAMPs)

Endogenous host structures released during cell stress or unprogrammed death—such as extracellular DNA, HMGB1, or hyaluronan fragments—that alert PRRs to damage.

Toll-like Receptors (TLR)

Germline-encoded pattern recognition receptors localized to cell surfaces and endosomes that recognize conserved microbial products.

C-type Lectin Receptors (CLR)

Calcium-dependent receptors—including Dectin-1, Dectin-2, CD206, and CD209—that target unusual fungal and bacterial carbohydrates to trigger phagocytosis.

NOD-like Receptors (NLR)

Cytosolic pattern recognition receptors, such as NOD1 and NOD2, that detect intracellular bacterial peptidoglycan fragments to induce inflammatory signaling.

RIG-I-like Receptors (RLR)

Cytosolic RNA sensors that detect uncapped viral RNA bearing $5'\text{-triphosphates}$ and signal via MAVS to activate IRF-mediated type I interferon production.

MyD88 and TRIF

Intracellular signaling adaptors for Toll-like receptors, where MyD88 activates $\text{NF-}\kappa\text{B}$ to promote inflammation and TRIF activates IRFs to drive interferon expression.

Pyroptosis

An inflammatory form of programmed cell death driven by inflammasome activation that releases proinflammatory cytokines into surrounding tissues.

Shedding Epithelium

A mechanical barrier mechanism in which epithelial layers undergo desquamation to clear attached or infected microorganisms from mucosal and skin surfaces.

Surfactant

A surface-tension-reducing substance in lung alveoli that acts as a chemical barrier by interrupting microbial membranes and denaturing pathogen proteins.

The Inflammasome

A cytosolic multiprotein complex (such as NLRP3) assembled in response to cellular stress, ROS, or bacterial products to cleave inactive pro-$\text{IL-}1\beta$ into active $\text{IL-}1\beta$.