Immunology Chapter 3 – Innate immunity: the induced response to
infection
Lines of defense
1. Barriers (see chapter 2)
2. Innate immunity: phagocytosis, complement, interferon, inflammation, fever
What plays a role?
1. Soluble molecules: the complement system
(See chapter 2)
2. Receptors: C-type lectin receptors and Toll-like receptors
3. Cells: neutrophils, macrophages, dendritic cells and NK cells
Macrophages: phagocytosis and killing of MO. Activation of T
cells and initiation of immune responses
Present in tissue
Big (macro) eater (phagocytosis)
Alert upon tissue damage and infection
Recognize non-self-structures
They express C-type lectin receptors (CLR): phagocytosis + no
signalling occurring.
They can be found only extracellular
o Mannose receptor
o Dectin-1
They express Toll-like receptors (TLR): no phagocytosis + signalling
occurs and therefore activation of cells occurs.
They can be found extracellular and intracellular: important
in viral infection because this happens inside the cell
o Toll-like receptor : bacteria, parasites – on the
membrane
o Toll-like receptor 3: viruses – in endosomes
o Toll-like receptor 4: bacteria – on the membrane
CLR on macrophages recognize carbohydrate
structure on pathogen surfaces the pathogens
are internalized by endocytosis fusion of
endosome with lysosome forms a phagolysosome
in which pathogens are degraded
TLR on macrophages recognize TLR ligands (present on
pathogens but not on the host, essential for pathogen survival,
structure remain equal during pathogens life, present on different
pathogens, ideal to distinguish self from non-self) signalling
occurs and therefore activation of cells occur. Important for
signalling are MyD88 and phosphorylation Leads to activation
and translocation of NFkB through degradation of its inhibitor and
inflammatory cytokine secretion via ER
Macrophages produce inflammatory cytokines (soluble proteins
which activates or changes other cells through binding of cytokine
infection
Lines of defense
1. Barriers (see chapter 2)
2. Innate immunity: phagocytosis, complement, interferon, inflammation, fever
What plays a role?
1. Soluble molecules: the complement system
(See chapter 2)
2. Receptors: C-type lectin receptors and Toll-like receptors
3. Cells: neutrophils, macrophages, dendritic cells and NK cells
Macrophages: phagocytosis and killing of MO. Activation of T
cells and initiation of immune responses
Present in tissue
Big (macro) eater (phagocytosis)
Alert upon tissue damage and infection
Recognize non-self-structures
They express C-type lectin receptors (CLR): phagocytosis + no
signalling occurring.
They can be found only extracellular
o Mannose receptor
o Dectin-1
They express Toll-like receptors (TLR): no phagocytosis + signalling
occurs and therefore activation of cells occurs.
They can be found extracellular and intracellular: important
in viral infection because this happens inside the cell
o Toll-like receptor : bacteria, parasites – on the
membrane
o Toll-like receptor 3: viruses – in endosomes
o Toll-like receptor 4: bacteria – on the membrane
CLR on macrophages recognize carbohydrate
structure on pathogen surfaces the pathogens
are internalized by endocytosis fusion of
endosome with lysosome forms a phagolysosome
in which pathogens are degraded
TLR on macrophages recognize TLR ligands (present on
pathogens but not on the host, essential for pathogen survival,
structure remain equal during pathogens life, present on different
pathogens, ideal to distinguish self from non-self) signalling
occurs and therefore activation of cells occur. Important for
signalling are MyD88 and phosphorylation Leads to activation
and translocation of NFkB through degradation of its inhibitor and
inflammatory cytokine secretion via ER
Macrophages produce inflammatory cytokines (soluble proteins
which activates or changes other cells through binding of cytokine
