Barriers, Immune Components, and the Complement System

A comprehensive vocabulary flashcard set covering barrier defenses, specialized immune cell types, lymphoid system structures, cytokines, and complement activation pathways based on the provided lecture transcripts.

Epithelial cells

Cells that line external barriers and internal surfaces of the body, arising from local stem cells at the site.

Antimicrobial peptides (AMPs)

Small peptides, such as defensins, that typically form pores in microbes and unfold microbial toxins.

Antimicrobial enzymes (AMEs)

Larger protein enzymes, such as lysozyme, that facilitate chemical reactions to degrade specific microbial biomolecules.

Commensal microbiota

Microbes that habitually colonize a host without causing disease, often displacing potential pathogens.

Opportunistic pathogens

Microbes (also known as pathobionts) that cause disease when the host immune system is weakened, such as Pneumocystis jirovecci in AIDS patients.

Lysozyme

An antimicrobial enzyme secreted onto mucosal surfaces and inside phagolysosomes that digests bacterial cell wall peptidoglycan linkages to expose the inner membrane.

Defensins

A family of small, amphipathic antimicrobial peptides found on epithelial barriers and in neutrophil granules that insert into exposed hydrophobic lipid bilayers to form pores.

Pro-defensins

The inactive precursor state of defensins in which the hydrophobic domain is blocked until cut by proteases made by alarmed immune cells or Paneth cells.

Endothelial cells

The primary cell type forming blood vessels, lymphatic vessels, and the heart, which carry out immune functions along barriers and blood vessels.

Hematopoiesis

The unidirectional and permanent development process in bone marrow where blood components are generated from a pluripotent hematopoietic stem cell (PHSC), guided by cytokines and adhesion molecules.

Phagocytes

Immune cells stationed under epithelial barriers that specialize in binding, engulfing, and destroying small microbes.

Granulocytes

Leukocytes that specialize in degranulation, releasing destructive or inflammatory mediators to control extracellular pathogens.

Lymphatic system

A network of vessels that collects fluid continually leaking into tissues and returns it to the bloodstream, while connecting secondary lymphoid tissues for lymphocyte patrolling.

Primary lymphoid organs

Tissues responsible for lymphocyte development, specifically the thymus for generating new naive T cells and the bone marrow for making new B cells.

Secondary lymphoid tissues

Meeting places, such as lymph nodes, tonsils, spleen, and Peyer's patches, where antigen-presenting cells present antigen to T and B cells to initiate adaptive immune responses.

White pulp

The region of the spleen that functions as a secondary lymphoid meeting place for T cells, B cells, and antigen-presenting cells to capture microbes from the bloodstream.

Red pulp

The region of the spleen responsible for filtering and removing old erythrocytes (red blood cells) from circulation.

Cytokines

Small signaling proteins produced by cells to communicate locally in a tissue or systematically with other distant cells.

Chemokines

A specialized type of cytokine that induces chemotaxis, directing cell movement toward higher concentrations of the attractant.

Complement system

An ancient system of soluble plasma proteins produced by the liver that circulate in blood and body fluids to attack extracellular microbes immediately upon barrier crossing.

C3b

A complement fragment with a short-lived exposed active thioester group that covalently binds to hydroxyl or amino groups on target surfaces to act as an opsonin tag.

Anaphylatoxins

Small complement cleavage fragments (C3a, C4a, C5a) that promote local inflammation, increase vascular permeability, and can cause smooth muscle constriction and circulatory collapse in excessive systemic amounts.

Opsonization

The process of tagging extracellular microbes or dying cells with proteins like C3b to enhance recognition and engulfment by phagocytic receptors such as CR1.

Membrane-Attack Complex (MAC)

A membrane pore structure formed by the assembly of C5b, C6, C7, C8, and multiple C9 proteins that causes target cell lysis by allowing water and sodium to rush in.

Alternative pathway

A complement pathway that initiates spontaneously and randomly through a low tickover rate, forming the soluble C3 convertase iC3bBb and cell-bound C3 convertase C3bBb.

Lectin pathway

A complement pathway initiated when pattern recognition receptors (MBL or Ficolins) bind microbial surface carbohydrates and activate MASPs to generate the C4b2a C3 convertase.

Classical pathway

A complement pathway initiated when C1q binds to IgM antibodies on a microbial surface, bringing C1r and C1s serine proteases to generate the C4b2a C3 convertase.

Mannose-binding lectin (MBL)

A soluble plasma pattern recognition receptor that leaks into infected tissue, binds mannose and fucose groups on microbes, and carries MASP serine proteases.

Protectin (CD59)

A complement-regulatory protein expressed on host cells that prevents the insertion of C9, blocking assembly of the Membrane-Attack Complex.

Decay Acceleration Factor (DAF)

A host cell surface complement-regulatory protein that disrupts and breaks apart the C3 convertase C3bBb.

Properdin (Factor P)

A soluble pattern recognition receptor secreted by neutrophils that binds MAMPs on pathogens or DAMPs on dying cells to stabilize the C3bBb convertase.