Inate Immunity Flashcards
Innate immunity definition:
Natural immunity that is present from birth.
Non-specific.
Innate immunity examples (5):
Physical barriers
Inflammatory mediators
Complement proteins
Acute phase proteins
Immune cells
Skin structure:
Tightly packed, highly keratinised cells.
Contains sebaceous glands which secrete hydrophobic oils, lysosomes and ammonia
Physiological factors of skin:
Low pH (5.5)
Low oxygen tension
Where do you find mucous membranes?
Line all body cavities that are in contact with the external environment
How does mucus kill pathogens?
Traps bacteria
Contains lysosomes and defensins that kill pathogens
What does commensalism bacteria do?
Competes with pathogens for resources and produce fatty acids and bactericidins that stops pathogens growing
What do interferons do?
Signal to uninflected cells to:
- Destroy RNA and reduce protein synthesis
- Undergo apoptosis
How are immune cells activated?
By interferons
What are cytokines?
Interferons released by virally infected cells
What do macrophages do?
Phagocytose bacteria
Phagocytosis process (7):
- PRRs binds to PAMPs on pathogen signalling formation of the phagocytic cup
- Cup extends around the pathogen and pinches off forming a phagosome
- Phagosome fuses with lysosome forming a phagolysosome
- Pathogen killed and contents degraded
- Debris released into extracellular fluid
- Pathogen-derived peptides are expressed on special cell surface receptors (MHC-II)
- Pro-inflammatory mediators released (TNF⍺) causing acute inflammation
How do innate immune cells recognise pathogens?
Pathogens express signature molecules not found on/in human cells called PAMPS
What does PAMPS stand for?
Pathogens associated molecular patterns
What does PAMPS stand for?
Pathogens associated molecular patterns
What are PRRs?
Pattern-recognition receptors on innate immune cells
What are MHC-II?
Special cell surface receptors
What is TNF⍺?
Pro-inflammatory mediator
Role of mast cells:
Deal with pathogens too large for phagocytosis
How do mast cells kill pathogens?
- PRRs on mast cell bind to PAMPs on pathogen
- Mast cell is stimulated to release pre-formed pro-inflammatory substances causing degranulation
(As this happens mast cell begins to produce new pro-inflammatory substances)
Examples of pro-inflammatory substances:
Histamine
Tryptase
What is transendothelial migration?
The recruitment of neutrophils to the site of infection/damage during acute inflammation
Transednothelial migration steps:
- Loss of intravascular fluid during inflammation causes slower blood flow, allowing neutrophils to migrate
- Neutrophils bind to adhesion molecules on the endothelial cells
- Neutrophils migrate across the endothelium via diapedesis
- Once in the tissues, the neutrophils travel to site of injury via chemotaxis
- Neutrophils are activated by PAMPs and pro-inflammatory mediators
Where do neutrophils travel in a vessel?
Close to endothelial cells of vessel
Killing mechanisms of neutrophils (3):
Phagocytosis
Degranulation
NETs
Phagocytosis in neutrophils:
Phagolysosomal killing via production of reaction oxygen species (ROS)
Degranulation in Neutrophils
Release of anti-bacterial granules
NETs in neutrophils:
Release of a net-like structure that traps pathogens, leading to phagocytosis
Modes of ingestion in neutrophils:
Endocytosis
Pinocytosis
Phagocytosis
Features of endocytosis in neutrophils:
Receptor mediated
Molecules that bind to membrane receptors are internalised
Important in adaptive immunity
Pinocytosis in neutrophils:
Ingestion of fluid of surrounding cells
What are Natural Killer (NK) cells?
Lymphocytes involved the rejection of tumors and virally infected cells
What do NK cells respond to?
Reduced levels of MHC class 1 in virally infected and cancerous cells
How to NK cells kill pathogens?
By degranulation
