Lecture 3, Innate Immunity Flashcards
What barrier is the first line of defense when a pathogen tries to enter our bodies?
Epithelium
What produces denfensins, and what do they do?
- Epithelial cells
- Use electrostatic interactions to enter lipid bilayer of pathogen -> permeabilization -> cell death
In a word, what’s the end result of the innate response?
Inflammation
What are the 4 main sx of inflammation?
- Rubor (redness)
- Calor (heat)
- Tumor (swelling)
- Dolor (pain)
What types of things are happening to the inflamed site of the body?
- Alteration of blood flow
- Increased vascular permeability
- Infiltration of white cells into area of reaction
In a word, what major category of cells is involved in the innate response?
Granulocytes
List some details of the 2 ways macrophages and neutrophils counter threats
Phagocytosis
- Particle uptake + employ receptors to enhance uptake of pathogens
- Receptor can bind PAMPS, complement and AB
Mediator production
- Cytokines and Chemokines
- Hydrolases
- Reactive oxygen and nitrogen species
What’s the difference b/w cytokines and chemokines?
- Cytokines: cause differentiation, proliferation, or death of other cells
- Chemokines: strictly recruit other types of cells
In the innate response, what receptor detects the “danger” signal?
What specifically does it detect?
Pattern recognition receptor (PRR) detects “danger” signal
- Patterns!
*What’s the difference b/w the DAMPs and PAMPs that the PRR is detecting?
- PAMPs: Pathogen Associated Molecular Pattern (foreign)
- DAMPs: Damage Associated Molecular Pattern (endogenous)
What occurs after a PRR binds a DAMP/PAMP?
*What large macromolecular structure forms to mediate this?
Leads to expression of proinflamatory cytokines and antimicrobial proteins
- Inflamasome
What are the 4 different classes of PRRs? (which are intra and which are extracellular?)
- Toll-like receptors (extracellular)
- C-type lectin receptors (extracellular)
- NOD-like receptors (intracellular)
- Rig-I-like receptors (intracellular)
What is mannose-binding lectin?
What organ produces it?
A soluble acute phase protein (like CRP) that’s produced by the liver (in response to IL-1, IL-6, TNFa) that binds mannose residues on pathogens, thus acting as an opsinin or complement activator
What are the 3 pw’s that lead to generation of C3 convertase during complement activation?
- Lectin pw
- Classical pw
- Alternative pw
*What does C3 convertase make and what are the 3 effects that can occur?
Makes C3b (bound to microbial surface), C3a (soluble)
- Recruit phagocytic cells to site of infection (C3a)
- Phagocytes engulf C3b-bound pathogen
- Membrane-attack complex (MAC) forms -> cell lysis
What 5 cells have phagocytic abilities?
Monocytes, Neutrophils, Eosionophils, Macrophages, Dendritic cells (doesn’t destroy)
What are the 2 classes of DCs?
Myeloid and lymphoid
Class II MHC is primarily used to present __________ antigens while Class I MHC molecules are major presenter of __________ antigens
- Exogenous
- Endogenous (peptides generated w/in the cells)
In what 3 ways do innate lymphoid (ILCs) cells differ from T/B cells?
(1) Absence of RAG gene—no DNA rearrangement
(2) Lack of myeloid cells/DCs marker
(3) lymphoid morphology.
What set of cells distinguishes the innate from adaptive immune systems?
Macrophages
Define opsonization, simply.
The coating of particles by molecules that enhance recognition by phagocytes
The final common path for pro-inflammatory activation is _____.
How is this commonly induced (simple, general mech).
NFkappaB
- PAMP binds PRR on immune cell.
Activation of transcription factor NF-kB activates genes encoding pro-inflammatory cytokines. One of the most important factors is IL-1 beta. Generation of IL-1beta also requires activation of a protein complex called ____________.
Inflamemasome
The inflamemasome’s function is to activate a protease called ____________, which cleaves precursor of what inflammatory cytokine to the mature form?
Caspase I
- IL-1beta
