MIMM 214 Lecture Notes - Lecture 9: Lymphopoiesis, Apoptosis, Complement System
Lecture 9 – January 23, 2017
Cytokines can imprint adaptive response
Cytokines Profile II
- Th1
o IFN – gamma
o Mostly acting on
▪ Macrophages
▪ Cytotoxic T cells
- Th2
o IL-4, IL-5, IL-10, IL-13
o Mostly acting on B cells
- Th17
o IL-17
o Pro-
o Inflammatory/autoimmunity
- Treg
o TGF, IL-10
- Take home
o Different T cells produce different cytokine patterns
o These patterns have specific impacts
o Do’t eorize these YET
Cimprints adaptive immune response
- Cell mediated immunity
o Directed to viral infection, intracellular pathogens
o Characterized by
▪ Macrophage activation
▪ Cytotoxic T lymphocyte activation
o Driven by Th1 cytokines
- Humoral immunity
o Directed to extracellular bacteria/pathogens
o Characterized by predominant B cell activation and antibody production
o Driven by Th2 cytokines
Cytokine Profiles I
- Different cytokines can induce differentiation of different cell types
- Different cell types then produce cytokines too
- Cytokines make T cells turn into certain type of T cell, then that specific T cell produces its own
cytokines which may or may not be the same type of cytokines that triggered its differentiation
Key cells and processes
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Inflammation: role of TNF-alpha
- Secreted by macrophages
- Stimulates
o Migration of innate cells
o Dilate blood vessels, increases clotting
Local vs Systemic effects
- TNF-alpha → local inflammation
o Macrophages only secret in certain spot
- Systematic TNF-alpha → systematic effects
o Lets say liver infection – attached to blood stream
o TNF-alpha all over body (systemic)
o Vasodilation everywhere
o Severe consequences
- SEPSIS: systematic infection and inflammation
o Coagulation all over
o Edema all over
o Can lead to death
Acute Phase response
- Induced by proinflammatory cytokines (IL-1, TNF-alpha, IL-6)
- Acute phase response involved:
o Increased synthesis/secretion of antimicrobial proteins from the liver
▪ Mannose-binding lectin (MBL)
▪ Complement components
▪ C-reactive protein → can opsonize bacteria and trigger classical complement
cascade
- Liver acute phase proteins activate other processes that help eliminate pathogens
Inflammatory cytokines have many effects
- IL-1beta, IL-6, TNF-alpha = key pro-inflammatory cytokines
- Effect on different tissues/cell types
o Acute phase response
o Mobilizing cells
o Fever
- Contributes to response against pathogen
- Note: fever caused by IL-1beta, Il-6, TNF-alpha, which signal to induce a cascade that leads to a
signal to hypothalamus → increase body temperature
Why is inflammation good/bad
- Good
o Complement
o Increased blood flow – vasodilation
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Document Summary
Ifn gamma: mostly acting on, macrophages, cytotoxic t cells. Il-4, il-5, il-10, il-13: mostly acting on b cells. Take home: different t cells produce different cytokine patterns, these patterns have specific impacts, do(cid:374)"t (cid:373)e(cid:373)orize these yet. Cell mediated immunity: directed to viral infection, intracellular pathogens, characterized by, macrophage activation, cytotoxic t lymphocyte activation, driven by th1 cytokines. Humoral immunity: directed to extracellular bacteria/pathogens, characterized by predominant b cell activation and antibody production, driven by th2 cytokines. Different cytokines can induce differentiation of different cell types. Different cell types then produce cytokines too. Cytokines make t cells turn into certain type of t cell, then that specific t cell produces its own cytokines which may or may not be the same type of cytokines that triggered its differentiation. Stimulates: migration of innate cells, dilate blood vessels, increases clotting. Tnf-alpha local inflammation: macrophages only secret in certain spot.