Innate Immune System Flashcards
Describe the differences in innate and adaptive immunity?
- Response time
- Specificity
- Memory responses
- Self/no self discrimination
- Soluble components
- Major cell types
- Main cytokine actions
What are the two types of barriers to infection in the innate immune system
What are physical barriers to infection?
What are epithelial barriers and the different types
What is mucus?
Where is it produced?
What is a special appendage used when in the respiratory tract?
What is mucus?
Where is it produced?
What other appendage is used to help?
Does mucus change based on the environment?
What are comensal microbes?
What help establish a relationship with these microbes?
What are AMPs
Where are AMPs found and what is their function?
Where else can AMPs be synthesized?
What receptors recognized pathogen?
What is being recognized on the pathogen?
What if its damaged self?
What are the 4 types of PRRs?
What do they do?
What is the composition of a TLR?
TIR domain = Toll/IL-1R
What is the myD88 pathway
MyD88 recruits IRAK1 (IL-1 receptor–associated kinase 1) and IRAK4.
IRAK1 phosphorylates itself and TRAF6 (tumor necrosis factor receptor–associated factor 6), activating it.
TRAF6 creates a scaffold that serves as an organizing center for subsequent signaling components.
The adapter proteins TAB1 and TAB2 (TAK1-binding proteins 1 and 2) bring associated TAK1 (transforming
growth factor-β-activated kinase 1) into proximity with IRAK1, which phosphorylates and activates
TAK1.
The IKK (inhibitor of κB kinase) complex, consisting of NEMO (NF-κB essential modifier),
IKKα, and IKKβ, is then recruited, enabling TAK1 to phosphorylate and activate IKKβ.
This leads to the final steps resulting in the activation of NF-κB.
Inactive NF-κB is retained in the cytoplasm byits IκB (inhibitor of NF-κB) subunit. Activated IKK phosphorylates IkB, leading to its degradation and the release of NF-κB, allowing it to enter the nucleus and activate gene expression.
TAK1 does double duty in this TLR signaling cascade. After separating from the IKK complex, it
activates MAPK signaling pathways that result in the activation of transcription factors including
Fos and Jun, which make up the AP-1 dimer.
Both NF-κB and AP-1 are essential for activating key
antimicrobial proteins and peptides as well as proinflammatory cytokines and chemokines that are
of key importance in the innate immune response.