Complement System and Leukocyte Extravasation

50 vocabulary flashcards covering key terms related to the complement system (Classical, Alternative, Lectin Mannose pathways, and their effects) and leukocyte extravasation from lecture notes.

Complement system

A system of 20 plasma proteins, primarily made in the liver, involved in immune defense.

Plasma proteins (complement)

A group of 20 proteins (B, C1-C9, D) involved in the complement system, 11 of which are used.

Liver

The organ responsible for synthesizing complement system proteins.

Classical Pathway

A complement activation pathway typically triggered by an Antigen-Antibody Reaction.

Antigen-Antibody Reaction

The specific trigger for activating the C1 complement protein in the Classical Pathway.

C1

The initial complement protein activated in the Classical Pathway, which then activates C4 and C2.

C146 Complex

A temporary complex formed during the Classical Pathway, involving activated C1, C4, and C2a.

C2

A complement protein cleaved into C2a and C2b in the Classical and Lectin Mannose pathways.

C3

A central and largest complement protein, cleaved into C3a and C3b, critical for various immune effects.

C3a

A complement product not typically used for convertase formation but involved in activating mast cells.

C3b

A complement product crucial for opsonization and forming C3 and C5 convertases in multiple pathways.

C5a

A complement product not typically used for convertase formation, but a potent chemoattractant for leukocytes.

C3 Convertase (Classical)

An enzyme complex (C4b2a or C1462a) that cleaves C3 into C3a and C3b.

C5 Convertase (Classical)

An enzyme complex (C4b2a3b or C1462a3b) that cleaves C5 into C5a and C5b.

MAC (Membrane Attack Complex)

A pore-forming complement complex (C5b6789) that ruptures bacterial cell walls, leading to cell lysis.

Alternative Pathway

A complement activation pathway triggered by bacterial endotoxin (LPS) and spontaneous hydrolysis of C3.

Bacterial Endotoxin (LPS)

A component of Gram-negative bacteria's cell wall that can trigger the Alternative Pathway of complement activation.

Spontaneous hydrolysis of Factor C3

An initial event in the Alternative Pathway, where C3 hydrolyzes to C3b, allowing Factor B to bind.

Factor B

A protein in the Alternative Pathway that binds to C3b, forming C3bB.

Factor D

A protease in the Alternative Pathway that cleaves Factor B when bound to C3b, forming C3bBb.

C3bBb (Alternative C3 Convertase)

An enzyme complex formed by C3b and cleaved Factor B (Bb) in the Alternative Pathway, which cleaves more C3.

Alternative C5 Convertase

An enzyme complex (C3bBb3b) formed in the Alternative Pathway that cleaves C5 into C5a and C5b.

Lectin Mannose Pathway

A complement activation pathway initiated when MBL binds to mannose residues on pathogen surfaces.

MBL (Mannose-Binding Lectin)

A protein synthesized in the liver that recognizes glucose and mannose residues in pathogen cell walls.

MASP (MBL-Associated Serine Protease)

A protease activated when MBL binds to pathogens, which then triggers C4 and C2 in the Lectin Mannose Pathway.

Neisseria, Candida, Salmonella

Examples of pathogens that have glucose and mannose residues in their cell walls, recognized by MBL.

Opsonization

An immune effect where C3b coats pathogens, activating neutrophils and macrophages for phagocytosis.

Cell lysis

The immune effect where the Membrane Attack Complex (MAC) ruptures bacterial cell walls.

Chemotaxis

The immune effect where C5a attracts neutrophils and macrophages to the site of infection.

Activation of MAST Cells

An immune effect where complement fragments C3a, C4a, and C5a trigger mast cells and basophils to release mediators.

Histamine

A chemical mediator released by activated mast cells and basophils, contributing to inflammation.

Serotonin

A chemical mediator that can be released by activated mast cells, contributing to inflammation.

Neutrophil Rolling (Extravasation)

The initial, weak adhesion phase of leukocyte movement out of blood vessels during inflammation.

Inflammation

A protective tissue response characterized by cytokine release, vasodilation, and leukocyte recruitment.

Cytokine release

A process during inflammation that changes expression of adhesion molecules on endothelial cells and leukocytes.

Vasodilation

Widening of blood vessels during inflammation, allowing neutrophils to react with the endothelium.

Leukocyte Recruitment

The process by which white blood cells are guided and brought to a site of inflammation or infection.

Chemokines

A type of cytokine that induces direct movement of cells, guiding leukocytes to infected tissues.

Endothelium

The inner lining of blood vessels, which interacts with leukocytes during extravasation.

Adhesion (leukocyte extravasation)

The process of leukocytes binding to endothelial cells, occurring in rolling and tight binding phases.

Selectins

Membrane glycoproteins expressed on activated endothelium that mediate the initial weak adhesion of leukocytes.

P-selectin

A selectin expressed rapidly on the surface of endothelial cells in response to histamine and TNF-α.

E-selectin

A selectin expressed later on endothelial cells' surface, induced by TNF-α and LPS.

ICAM (Intracellular Adhesion Molecule)

Single-pass membrane proteins (ICAM-1, ICAM-2) on endothelial cells that allow tighter adhesion of leukocytes.

Leukocyte Integrins

Alpha and beta protein chains on leukocytes whose conformational change allows tighter binding to ICAMs.

Extravasation

The overall process of leukocytes migrating out of blood vessels into inflamed or infected tissues.

Rolling Adhesion

The initial weak adhesion phase of extravasation, where leukocytes loosely bind to selectins on the endothelium.

Tight Binding

The phase of extravasation where leukocytes stop rolling and strongly adhere to the endothelium via integrins and ICAMs.

Diapedesis

The process where a leukocyte crosses the endothelial walls and penetrates the basement membrane to enter subendothelial tissue.

Migration (leukocyte)

The final stage of extravasation where leukocytes follow chemokine concentration gradients to deeper tissues.