L1.2 Innate immunity Flashcards
1
Q
Immunity
A
- the ability of an organism to resist a particular infection or toxin by the action of specific antibodies or sensitized white blood cells
- Characterised by: Hyperaemia, oedema, pain, leukocyte infiltration, loss of function
2
Q
Inflammation
A
- characterised by heart, redness, swelling, pain, loss of function
3
Q
Innate immunity overview
A
- Always takes effect through pro-inflammatory cytokines
- Quick, No memory
- Slash/Burn → resolves
- Through neutrophils
4
Q
Adaptive immunity overview
A
- Works together with innate
- Slow, flexible, have memory & recall
- Amplify/kill/clear → Long-term memory
5
Q
Pattern recognition receptors (PRR)
A
- Toll-like receptors (1-11) - recognise: bacteria/viruses…
- Expressed in sentinel cells (i.e. macrophages/dendritic cells)
- NOD/NLR - recognise: DNA from bacteria
- RLR - recognise: viruses
- CLR (C-type lectin/AKA Dectins) - recognise: fungi
- There are 7 reused domains of PRR.
6
Q
Evolution of the immune system
A
- The immune system has evolved to discriminate b/w infectious non-self & non-infectious self
7
Q
Mounting an appropriate response
A
- Recognise (self from non-self)
- Kill/Contain (the inflammatory response)
- *contain = putting a fibrous shell around it
- Resolve (organ protective catabasis)
- Decline of diseases by turning off inflammation
8
Q
Overview of infection + defense
A
- Bacterial adhesion to epithelium
- Local infection, penetration of epithelium (if skin is broken)
- Induces wound healing
- Local infection of tissues - initiates adaptive immunity through:
- Activation of macrophages
- Dendritic cells migrating to lymph nodes
- Adaptive immunity
9
Q
Barriers of innate immunity
A
- Mechanical:
- Movement of mucus by cilia
- Chemical
- FA, enz, HCl
- Microbiological
- Metagenome (our genome + bacteria genome)
- Could defend from other bacteria
- Metagenome (our genome + bacteria genome)
10
Q
Signal transduction from PRRs
A
*IRF = interfereron regulatory factor*
11
Q
TLRs
A
- Have similar structures, but sense different things → ultimately producing similar effects
- All signals converge to NFK-β and produce type I interferon response
- Can be monomers/complexes/heterodimers
- Evolved to recognise specific molecules
- e.g.
- Toll 4 complex recognises LBP/LPS → NFK-β → produce pro-inflammatory cytokines
- Toll 3, 7, 9 complexes recognise viruses → NFK-β → produce pro-inflammatory cytokines
12
Q
Important cytokines
A
13
Q
Activated neutrophils
A
- Attack & destroy bacteria by slash & burn destructive proteases & oxidants
14
Q
Progressive activation of leukocytes
A
- Endothelium irritated → produce endothelial chemoattractants → capture leukocytes → roll → *if insult is severe → firm adhesion → transmigration b/w cells (other chemoattractants in tissues)
15
Q
What is the pattern of WBC controlled by
A
- selectins & integrins
16
Q
Example of specific ligands & R. controlling movement of WBC in the body
A
- e.g. CCL8 (interleukin 8 - a ligand) works through CCR5.R → mobilises WBC to move from blood to tissues
17
Q
How is apoptosis achieved?
A
- Cell sustains irreparable damage (e.g. excessive DNA damage) → signaled to undergo apoptosis
- Macrophages eat cell & removes (process kept inside cell)
- Phagocytosis prevents inflammation
- Is anti-inflammatory, PRO-resolution
- Macrophages eat cell & removes (process kept inside cell)
18
Q
How is necrosis achieved?
A
- Serious chronic inflammation
- → overwhelmed by tissues cell death
- → necrotic cell released outside
- → leads to serious inflammation (detrimental) by releaseing toll agents (HMGBP, RAGE) → activates toll R.
19
Q
What are the pro-resolution processes?
A
- Clearance of pathogens
- ↓ key signals for WBC → cell apoptose
- Efferocytosis (removing apoptic cells)
- Turns on local anti-inflammatory factors to help tissues back to healed state
20
Q
Do steroids affect the innate immunity?
A
- Do not affect innate immunity
