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non-inflammatory phagocytosis

process in which phagocytic cells engulf cells that die via apoptosis; for maintenance of our own tissue

inflammatory phagocytosis

host defense process mediated by phagocytic cells

antigen presenting cells

internalize pathogens, degrade them into little pieces, and take small peptides and display them on MHC molecules and this is what T-cells recognize.

examples of APCs

macrophages, B-cells, dendritic cells

link from innate immunity to adaptive immunity

action of antigen presenting cells


enzymes that chew up collagen and proteins that are involved in junction adhesion to make it easier to move into the surrounding tissue


involved in pulling the cells through the system/junctions


mediated by complement molecules, chemokines, and other small molecules which tell cells where to go once they have gotten through the endothelial cell layer

professional phagocytes

neutrophils and monocytes/macrophages

non-professional phagocytes

epithelial and endothelial cells

Fc Receptors and Complement Receptors

essential for efficient phagocytosis

Fc receptors

proteins found on a variety of leukocytes that bind to the Fc portion of antibodies; transduce intracellular signals , Cell-surface receptors for the Fc portion of some immunoglobulin isotypes. They include the Fcγ and Fcɛ receptors.


complement receptor on phagocytic cells; consists of short consensus repeats; bind to multiple ligands; does not mediate phagocytosis alone - needs help


complement receptor on phagocytic cells; can mediate phagocytosis alone with stimulation; have alpha and beta chains

opsonized antigen

a bacterium that already has antibodies made for it


An immune response in which the binding of antibodies to the surface of a microbe facilitates phagocytosis of the the microbe by a macrophage


phagocytic cells

stages of phagocytosis

ligand binding, activation of phagocytic cell, engulfment, internalization/fusion with lysosomes, bacterial killing

ligand binding

Fc receptors on leukocytes bind with Fc portion on antibodies (that is bound to antigen)

activation of phagocytic cell

mediated by ligand binding and activation of phagocytic cell through other receptors such as cytokines, LPS, chemoattractants, etc.


when phagocytic cell comes in with all of its receptors for different ligands that match the antibodies, it enables the phagocytic cell to zip around the pathogen and internalize it; this process is driven by receptors on phagocytic cell; dramatic change in the cytoskeleton of the cell

internalization/fusion with lysosomes

formation of the phagolysosome, an acidified vesicle suited for pathogen destruction

zipping up process

pseudopodia extend around the pathogen where the selectins and integrins run along the side of the pathogen; involves also actin filaments and myosin for motility and cytoskeletal changes.

Respiratory burst - NADPH Oxidase System

a series of membrane associated enzymes that form free radicals which kill pathogens by disrupting the structure of their proteins

free radicals

superoxide anion, hydrogen peroxide


found in azurophiic granules; mediated generation of HOCl (bleach/Dakin solution) which kill pathogens

enzymes generated by the Respiratory Burst-NADPH Oxidase system

Nitric oxide, myeloperoxidase, superoxide anion, hydrogen peroxide

azurophilic granules

contain elastase, cathespins, lysozymes, meeloperoxidase, and other enzymes that degrade the phagocytosed pathogen

neutrophil extracellular traps (NETs)

when neutrophils are fully activated and have done some phagocytosis, they undergo this process where their nuclear membrane dissolves to release chromatin and granular proteins that form extracellular fibers than bind, trap, and kill bacteria (Gram + and Gram -)

chronic granulomatus disease

genes missing or mutated in the NADPH oxidase system of phagocytosis

chediak-higashi syndrome

membrane trafficking problems, poor fusion of lysosomes and other organelles

clinical presentation of chronic granulomatus disease

recurrent bacterial and fungal infections

clinical presentation of chediak-higashi syndrome

pigmentation abnormalities adn recurrent skin and respiratory infections

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