Immunity Overview: Innate and Adaptive Immunity (Chapter 1-9 Notes)

A vocabulary-style set of flashcards covering innate vs. adaptive immunity, barriers, the complement system, normal microbiota, and key immune components and processes mentioned in the lecture notes.

Innate immunity

The nonspecific part of the immune system; fast, memoryless defense present at birth; includes barriers, inflammation, fever, and the complement system.

Adaptive immunity

Specific immune response mediated by B cells and T cells; develops memory for long-term protection and responds more quickly upon re-exposure.

First line of defense

Barriers that prevent pathogen entry, including mechanical and chemical barriers and normal microbiota.

Second line of defense

Non-specific responses such as inflammation, fever, and the complement system that activate after entry of a pathogen.

Mechanical barriers

Physical processes that help remove invaders, e.g., urine flow and tears.

Chemical barriers

Substances associated with skin and mucous membranes that deter pathogens (e.g., skin secretions, sweat, salty environment).

Inflammation

Localized innate response to injury or infection, aimed at containment and healing.

Fever

Systemic increase in body temperature as part of the innate response to infection.

Complement system

A cascade of plasma proteins that enhances immune responses; activation leads to opsonization, membrane attack complex, inflammation, and chemotaxis.

Normal microbiota

Resident microorganisms that form a barrier by occupying niches and secreting antibacterials like bacteriocins.

Mucous membranes

Lining of open body surfaces that trap pathogens with mucus and remove them via cilia or coughing.

Goblet cells

Epithelial cells that secrete mucus to trap microbes in mucous membranes.

Endothelium

Simple squamous lining of blood and lymphatic vessels; held together by tight junctions to prevent entry of pathogens.

Tight junctions

Connections between adjacent endothelial cells that prevent paracellular passage of pathogens.

Blood-brain barrier

Selective endothelial barrier protecting the brain and spinal cord from many pathogens.

Keratinized epidermis

Outer skin layer rich in keratin; provides dry, waterproof barrier and limits pathogen entry.

Sebaceous glands

Oil-secreting glands that produce sebum, coating follicles to hinder pathogen access.

Sebum

Oily secretion that helps seal hair follicles and restrict microbial entry.

Sweat glands

Glands that produce sweat with antimicrobial components, reducing microbial growth.

Dermacide

Antimicrobial component in sweat that inhibits bacteria and fungi.

Acute phase protein

Plasma proteins whose levels rise during inflammation to help fight infection.

C-reactive protein (CRP)

An acute-phase protein indicating inflammation; helps inhibit bacterial growth and trap pathogens.

Ferritin and transferrin (iron sequestration)

Proteins that bind iron to limit bacterial growth by depriving pathogens of this nutrient.

Fibrinogen

Plasma protein that initiates clotting to wall off infection and impede pathogen spread.

Opsonization

Coating of a pathogen by antibodies or complement to enhance phagocytosis.

Membrane attack complex (MAC)

Complement-formed pores inserted into a target cell’s membrane, causing lysis.

Chemotaxis

Movement of immune cells toward a chemical signal released during immune responses.

Cytolysis

Destruction of a cell due to pore formation in its membrane (e.g., MAC).

Antigen

Substance that provokes an immune response and is recognized as foreign by the immune system.

Antibody

Proteins produced by B cells that specifically bind antigens.

B cells

Lymphocytes that differentiate into plasma cells to produce antibodies (humoral immunity).

T cells

Lymphocytes involved in cellular immunity; include cytotoxic and helper T cells.

Humoral immunity

Adaptive immune arm involving B cells and antibodies.

Cellular immunity

Adaptive immune arm involving T cells and their direct actions against infected cells.

Memory

Part of adaptive immunity where previous exposure leads to faster and stronger responses upon re-exposure.

Adaptive response timeline

First exposure can take about 1–2 weeks to become fully functional; memory responses are faster.

Phagocytosis

Engulfing and digesting pathogens by phagocytes, often enhanced by opsonization.