Innate Immunity Flashcards

(35 cards)

1
Q

describe the timeframe and the sequence of events in the innate response

A

immediate: 0-4 hours

infection –> recognition by preformed, nonspecific effectors –> removal of pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

describe the timeframe and sequence of events in the early induced innate response

A

early: 4-96 hours

infection –> recruitment of effector cells –> recognition of PAMPs, activation of effector cells and inflammation–> removal of pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

describe the timeframe and sequence of events in the adaptive response

A

late: >96 hours

infection –> transport of antigen to lymphoid organs –> recognition by naive B and T cells –> clonal expansion and differentiation to effector cells–> removal of pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the protective immunity against pathogen in the interstitial spaces, blood, and lymph?

A

Complement
Phagocytosis
Antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the protective immunity against pathogen on epithelial surfaces?

A

Antimicrobial peptides

Antibodies, especially IgA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the protective immunity against pathogen in the cytoplasm?

A

NK cells

Cytotoxic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the protective immunity against pathogen in vesicles?

A

T cell and NK cell dependent macrophage activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is released by epithelial cells and what does it do?

A

Defensin - highly charged, will infiltrate the cell membrane and form a pore

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the general characteristics of inflammation?

A

triggered by innate cells that generate inflammatory mediators

tries to destroy or contain pathogen

orchestrates repair of damaged tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the effects of inflammation?

A

calor, dolor, tumor, rubor

alteration of blood flow

increased vascular permeability

infiltration of white cells into reaction area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Discuss the main functions and locations of Macrophages/Monocytes

A

monocytes: blood
macrophages: tissue

first responder, long lived

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

discuss the main functions and locations of neutrophils

A

most common circulating white blood cell

short lived

rapid responder

rarely found in normal tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do macrophages and neutrophils counter threats?

A

phagocytosis and mediator production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

discuss phagocytosis

A

uptake of particles via receptors that can bind PAMPS, antibody, or complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the mediators that are release by macrophages and neutrophils?

A

cytokines, chemokines, hydrolases, reactive oxygen and nitrogen species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

differentiate between cytokines and chemokines

A

cytokines: can promote differentiation, proliferation, or recruitment of other cells
chemokines: only recruit other cells

17
Q

What is the detector of the “danger” signal in the immune response?

A

Pattern recognition receptor (PRR)

18
Q

What are the danger signals that PRRs recognize?

A

PAMPS (pathogen associated molecular pattern) - foreign

DAMPS (damage associated molecular pattern) - endogenous

19
Q

What occurs with binding of PAMPS/DAMPS?

A

expression of proinflammatory cytokines and antimicrobial proteins

20
Q

What are the four classes of PRRs and where are they expressed?

A

Toll-like receptors (TRRs) - cell surface

NOD-like receptors - intracellular

C-type lectin receptors - cell surface

Rig-I-like receptors - intracellular

21
Q

How are TLRs activated?

A

TLRs can bind multiple targets (not like Ab), diversity is preset

22
Q

what are the differences between PRRs and Ab?

A

Diversity: TLRs have preset binding capabilities against general epitopes (flagella, etc.), and we only have ~100s of them –> PRR recognize unique repeated structures

Ab are specific for a very specific epitope and we can generate millions of different specificities via ecombination

23
Q

Explain what happens after activation of a PRR in the context of the inflammasome

A

activation of PAMPS or DAMPS activate cascades that lead to the activation of the inflammasome, which activates caspase-1 to cleave pro-IL-1Beta and pro-IL-18 to IL-1Beta and IL-18 which are cytokines that are released to stimulate the inflammatory response

24
Q

What does C-type lectin recognize on pathogen?

A

The PRR C-type lectin on phagocytic cells recognize terminal mannose on pathogen glycoprotein

25
What else can bind pathogen mannose?
Mannose binding lectin (MBL)
26
How does MBL activate complement?
Binding to mannose results in a conformational change, leading to activation of c3 convertase which cleaves c3 leaving c3 bound to the microbial surface and the release of c3a
27
What is the function of c3a?
c3a and c5a recruit phagocytic cells to the site of infection and promote inflammation
28
what is the function of c3b?
c3b is recognized by phagocytes with that specific receptor, which phagocytize and destroy the pathogen
29
what is the ultimate result of complement?
formation of the MAC (membrane-attack complex (c5b, c6, c7, c8, c9)) which forms a pore resulting in cell lysis
30
What is an important general function of c3b?
It is a bridge to adaptive immunity (phagocytosis)
31
how does the phagolysosome kill ingested material?
release of superoxide via NADPH
32
What are the general functions of dendritic cells?
Very good APCs --> present Ag to T cells multiple PRRs roam freely high phagocytic activity do not promote inflammation
33
what kind of antigen does MHC class I primarily present?
present peptide generated within the cell
34
what kind of antigen does MHC class II primarily present?
exogenous antigen
35
What are innate lymphoid cells and how are they different from T/B cells?
there are 3 groups of ILCs: they use PRR and produce cytokines 1. have no RAG gene 2. lack of myeloid cells/don't have DC marker 3. lymphoid morphology