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Host Defense Exam 1 > Innate Immunity > Flashcards

Innate Immunity Flashcards

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

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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

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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

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4
Q

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

A

Complement
Phagocytosis
Antibodies

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5
Q

What is the protective immunity against pathogen on epithelial surfaces?

A

Antimicrobial peptides

Antibodies, especially IgA

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6
Q

What is the protective immunity against pathogen in the cytoplasm?

A

NK cells

Cytotoxic cells

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7
Q

What is the protective immunity against pathogen in vesicles?

A

T cell and NK cell dependent macrophage activation

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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

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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

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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

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11
Q

Discuss the main functions and locations of Macrophages/Monocytes

A

monocytes: blood
macrophages: tissue

first responder, long lived

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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

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13
Q

How do macrophages and neutrophils counter threats?

A

phagocytosis and mediator production

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14
Q

discuss phagocytosis

A

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

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15
Q

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

A

cytokines, chemokines, hydrolases, reactive oxygen and nitrogen species

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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
Q

What else can bind pathogen mannose?

A

Mannose binding lectin (MBL)

26
Q

How does MBL activate complement?

A

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
Q

What is the function of c3a?

A

c3a and c5a recruit phagocytic cells to the site of infection and promote inflammation

28
Q

what is the function of c3b?

A

c3b is recognized by phagocytes with that specific receptor, which phagocytize and destroy the pathogen

29
Q

what is the ultimate result of complement?

A

formation of the MAC (membrane-attack complex (c5b, c6, c7, c8, c9)) which forms a pore resulting in cell lysis

30
Q

What is an important general function of c3b?

A

It is a bridge to adaptive immunity (phagocytosis)

31
Q

how does the phagolysosome kill ingested material?

A

release of superoxide via NADPH

32
Q

What are the general functions of dendritic cells?

A

Very good APCs –> present Ag to T cells

multiple PRRs

roam freely

high phagocytic activity

do not promote inflammation

33
Q

what kind of antigen does MHC class I primarily present?

A

present peptide generated within the cell

34
Q

what kind of antigen does MHC class II primarily present?

A

exogenous antigen

35
Q

What are innate lymphoid cells and how are they different from T/B cells?

A

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

Host Defense Exam 1 (13 decks)

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