Unit 1 – Introduction to Immunology and Innate Immunity

A set of vocabulary flashcards covering core concepts from Unit 1: Introduction to Immunology, innate immunity, and the complement system.

Immunity (modern definition)

All physiologic mechanisms that enable the host to recognize materials as foreign and to dispose of them with or without injury to its own tissues.

Immunity (early/old definition)

Resistance of the host to reinfection by a given microorganism.

Acquired immunity

resistance to reinfection; responses developed after exposure to a pathogen.

Innate Immunity

Non-specific defenses, immediate protection, first line of defense against infection.

Adaptive Immunity

develops after exposure to a pathogen; humoral and cell-mediated components.

Humoral Immunity

Antibody-mediated immunity; extracellular pathogens.

Cell-Mediated Immunity (CMI)

T cell–mediated responses; direct cell-to-cell contact or cytokine signaling; defends against intracellular pathogens and tumor cells.

Immunomodulation

Regulation of immune response by infections, drugs, or environmental cues.

Self vs non-self recognition

immune system distinguishes host tissues from foreign materials and mounts responses to non-self.

Pattern Recognition Receptors (PRRs)

Receptors on immune cells that recognize microbial patterns (PAMPs) or danger signals (DAMPs) to activate innate immunity.

Pathogen-Associated Molecular Patterns (PAMPs)

Molecular structures common to groups of pathogens recognized by PRRs.

Damage-Associated Molecular Patterns (DAMPs)

fragments released by damaged or dying cells that activate innate immune responses.

Toll-like Receptors (TLRs)

PRRs that detect PAMPs and trigger cytokine production and inflammation.

Scavenger Receptors (SR)

PRRs that bind lipids and other ligands to promote phagocytosis.

NOD-like Receptors (NODs)

Intracellular PRRs that sense bacterial components to activate inflammatory responses.

C-type Lectin Receptors (CLR)

PRRs see carbohydrates on pathogens to modulate immunity.

RIG-I-like Receptors (RLR)

Cytosolic PRRs that detect viral RNA and induce antiviral responses.

Lipopolysaccharide (LPS)

Endotoxin; PAMP from Gram-negative bacteria that stimulates inflammation when recognized by PRRs.

Flagellin

Protein of bacterial flagella, PAMP by immune receptors.

Mannose

Carbohydrate structure on pathogens recognized as a PAMP by immune receptors.

Zymosan

Yeast cell wall component recognized as a PAMP by the immune system.

Viral RNA

Genetic material of viruses detected by innate immune sensors as a PAMP.

Antibody-Mediated or Humoral Immunity

antibodies produced by B cells; defense against extracellular pathogens.

Cell-Mediated Immunity Targets

Primarily targets intracellular pathogens and tumor cells.

First Line of Defense (Innate External Barriers)

External barriers such as intact skin and mucosal surfaces that limit infection.

Mucosal Defenses

Respiratory, gastrointestinal, and urogenital tracts with mucus, cilia, saliva, and tears containing antimicrobial factors.

Goblet Cells and Mucus

Goblet cells secrete mucus to trap pathogens on mucosal surfaces.

Secretory Antimicrobial Products

Secretions (e.g., sebaceous sebum, lactic acid) that reduce pathogen survival on surfaces.

Iron-Binding Proteins (Lactoferrin, Transferrin)

Bind iron to limit microbial growth and support innate defense.

Reactive Oxygen Intermediates (ROIs)

Oxygen-derived molecules made during phagocytosis that kill pathogens.

Natural Killer (NK) Cells

Innate lymphocytes that lyse virus-infected and tumor cells without antigen-specific receptors.

Phagocytosis and Phagolysosome

Ingestion of pathogens to form a phagolysosome where killing occurs via ROS and enzymes.

Inflammation

Nonspecific, cytokine-mediated response to injury or invasion with redness, heat, swelling, and pain.

Fever and Cytokines

Systemic rise in temperature driven by cytokines (IL-1, IL-6, TNF-α) that inhibits pathogen growth.

Acute-Phase Proteins

Liver-synthesized plasma proteins that rise or fall during inflammation and help drive the response.

C-Reactive Protein (CRP)

Acute-phase pentraxin; marker of infection and inflammation.

Erythrocyte Sedimentation Rate (ESR)

Nonspecific indicator of inflammation based on red blood cell settling rate.

Complement System

30 serum proteins that aid immunity; activated via three pathways to defend against microbes.

C3 – Heart of the Pathways

Central component of all three complement pathways; cleaved to C3a and C3b.

Membrane Attack Complex (MAC)

Terminal complement complex (C5b6789) that forms pores and lyses target cells.

Opsonization

Coating of pathogens with C3b or antibodies to enhance phagocytosis.

C3 Convertases

Enzyme complexes that cleave C3; classical/lectin: C4b2a; alternative: C3bBb.

C5 Convertases

Enzyme complexes that cleave C5 to C5a and C5b; formed by C4b2a3b or C3bBb3b.

Anaphylatoxins

(C3a, C4a, C5a) promote inflammation and recruit immune cells

Properdin (Factor P)

Stabilizes C3 convertases, extending their activity on microbial surfaces.

C1 Complex (C1qrs)

Initiator of the classical pathway; C1q binds antibodies; C1r and C1s propagate the cascade.

What do probiotics do for our immunity?

live strains of bacteria that promote growth of other health microbiota

what do prebiotics do for our immune system?

non soluble fiber that supports the lining of the gut and growth of bacteria

define efferocytosis

Process of ingesting apoptotic cells, clearing dead cells and prevents autoimmunity so apoptotic cell membranes DO NOT rupture by secondary necrosis

chemotaxis

Movement of immune cells towards a chemical signal, guiding them to sites of infection or inflammation.

extravasion

neutrophil rolls endothelium, arrests itself, and moves into the tissue

exocytosis

release of reactive oxygen molecules, debris and can damage nearby cells/tissue

What is the respiratory burst?

killing & digestion of pathogens by the release of reactive oxygen species; hydrogen peroxide, hydroxide, superoxide

What do hepatocytes do?

acute phase proteins synthesized in the liver

What is the amplification loop of the complement system?

C3b and B is bound on the membrane and when activated by factor D becomes C3 convertase that can keep clipping more C3b and C3a

Compare the CRP test to the ESR test

CRP levels are higher in plasma during infection and acts as an opsonin to prepare debris for phagocytosis, PRO inflammatory

ESR is an EARLY INDICATOR or inflammation because proteins (fibrinogen) coat RBCs and make them clump together and fall faster ONLY TESTED EARLY, NOT TRACKED

Compare inducible vs noninducible defense mechanisms

inducible must be “turned on” when needed while non inducible is “on” at all times

What are the characteristics of an immune response?

What are the 4 types of acquired immunity?

Compare cellular vs humoral

cellular is cell mediated, direct cell to cell contact or the production of cytokines

defends against INTRACELLULAR pathogens and cancerous cells

humoral is antibody mediated, in body fluids and defends against EXTRACELLULAR pathogens

What are defensins and what do they do?

neutralize toxins and disrupt microbial patterns, cause lysis and release granules

What are the physiological factors in host defenses?

body temp, oxygen tension, nutrition, malnutrition, stress, exercise, microbiota, hygiene

How does iron contribute to innate immunity?

iron causes formation of reactive-oxygen intermediates

What is the hygiene hypothesis?

early exposure helps “program” immune system

paneth cells secrete angiogenin-4

B cell development in peyers patches

stim B cell differentiation

Granulocytic phagocytes

neutrophils, eosinophils, basophils

What are the two pools of PMNs

marginated - leukocyte rolling which wait to get attached into tissue during stress/infection demarginate to join the circulating pool

circulating - always ready to move into the cell and circulate in CBC

Examples of mononuclear cells

monocytes, macrophages, NK cells,

Examples of opsonins

complement system, pentraxins, antibodies

phagocytes need these to stop bacteria from escaping

define zymogen

enzymes inactive until cleaved

what are the effects of complement activation?

lysis of bacteria & enveloped viruses by MAC

C3b mediates opsonization through complement fixation

Discuss clinical features that cause elevated/decreased complement protein concentrations