Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immunology and Infection > Innate Immune System > Flashcards

Innate Immune System Flashcards

1
Q

what are the properties of the early immune system response?

A
  • starts when a microbe is encountered
  • not highly specific
  • fast
  • resolves without creating a memory
  • aim is to clear the pathogen/infected cells and alert the adaptive response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the 4 general principles of the immune response?

A
  1. clear the microbe/inhibit its replication
  2. process microbes and present to cells of the adaptive immune system
  3. alert and attract other cells
  4. kill itself
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how might the microbe be cleared or its replication inhibited?

A

phagocytosis, interferon system

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

what is the name of the process where microbes are presented to cells of the adaptive immune system?

A

antigen processing and presentation

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

how might cells in the immune system alert and attract other cells?

A

upregulation of surface receptors, cytokines and chemokines

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

how will an infected cell kill itself?

A

apoptosis

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

what cells have the potential to perform the activities listed in the general principles of the immune response?

A
  • all cells
  • some cells are specifically made and programmed
  • exceptionally good at the first 3 they are the cells of the innate immune system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is inflammation the result of?

A
  • result of infection (a physiological process)

- damage of a tissue

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

why is inflammation needed?

A

pre-requisite of a successful immune response

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

what are the features of inflammation?

A

heat, redness, swelling and pain

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

what are the 3 roles of inflammation?

A
  1. delivery of effector cells/moleucles to the site of infection; enhance microbe clearnace
  2. blood clotting to form a physical barrier and prevent spreading of infection to the bloodstream
  3. enhancement of the tissue repair process
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what changes are there in the blood vessel during inflammation?

A
  • increased vessel diameter
  • increased adhesion molecules to bind leukocytes
  • increased vascular permeability (leaky)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how do leukocytes move into bloodvessels?

A

attachment followed extravasation

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

how fast is the innate immune response?

A

happens within hours

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

what are neutrophils?

A
  • form the plolymorphonuclear cell family with basophils and eosinophils
  • most abundant type of white blood cells
  • predominant cells in pus
  • first to arrive
  • quick, short lived and motile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how do neutrophils kill?

A
  • phagocytosis
  • degranulation
  • neutrophil extracellular traps (NETs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what does phagocytosis require?

A

substantial membrane rearrangement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the 5 steps in phagocytosis?

A
  1. attachment/adhesion and engulfment
  2. phagosome formation
  3. recruitment of lysosome
  4. phagosome-lysosome fusion produces a phagolysosome
  5. microbe is killed with high concentration of reactive oxygen species, defensins, hydrolytic enzymes and the low pH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is degranulation?

A

release of azurophilic or specific granules containing proteases, defensins and reactive oxygen species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are NETs?

A
  • primarily composed of DNA and anti-microbial proteins
  • acts by trapping bacteria, killing them through localised and high concentrations of anti-microbial proteins
  • NETs essentially releases their chromatin to create a sticky environment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are macrophages?

A
  • myeloid lineage, mature from monocytes

- reside in tissues, already there before a threat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what does the macrophage tissue in infected tissue?

A

-phagocytse microbes while circulating monocytes are recruited to the tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how do macrophages become activated?

A

through direct interaction with pathogens or through factors secreted by T helper lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the functions of macrophages?

A
  • highly phagocytic (engulf and destroy a pathogen)
  • secrete cytokines (orchestrate the inflammatory response)
  • present antigens to T cells
  • contribute to tissue repair and formation of new blood vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are dendritic cells?

A
  • myeloid and plasmocytoid dendritic cell
  • have long finger like processes
  • migrate from the bloodstream to the tissue or are tissue resident
  • are phagocytic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what happens to dendritic cells during maturation?

A
  1. become less phagocytic and endocytic
  2. proliferate
  3. process microbial proteins to small peptides that can be recognised by T lymphocytes
  4. upregulate expression of surface proteins and cytokines required for antigen presentation
  5. secrete type 1 interferons that inhibit pathogen replication
  6. go to the nearest lymph node to present to T cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are plasmocytoid dendritic cells?

A
  • subset of DC’s derived from CLP that look like plasma cells
  • rare less than 0.5% of white blood cells
  • mainly produce type 1 interferons
  • very important in antiviral response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are innate lymphoid cells?

A
  • dont sense antigens directly they are activated by signal cytokines
  • produce effector proteins
  • dont have an antigen specific receptor
  • mirror the phenotype and function of T cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are natural killer cells?

A
  • terminally differentiated cell of the lymphoid lineage
  • large
  • characterised by cytoplasmic granules and cytotoxic proteins
  • also secrete IFNy and kill infected cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

how do natural killer cells become activated?

A

in response to type 1 interferons secreted by other innate cells of cytokines produced by the tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how is the cytotoxic activity of natural killer cells controlled?

A

through inhibitory and activating receptors on the cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are the main functions of the natural killer cell?

A
  • clearance of missing self cells

- antibody dependent cellular cytotoxicity

33
Q

what is meant by missing self when referring to natural killer cells?

A
  • body cells express MHC-1, how cells are recognised as self
  • pathogens down-regulated MHC-1 to avoid clearance
  • NKs kill any cell with no/low MHC-1 expression
  • MHC-1 have a cargo (peptide) that can be self or microbial
34
Q

what is antibody dependent cellular cytotoxicity?

A
  • NK cells also carry receptors for the Fc region of antibodies
  • microbes/cells coated with antibodies can trigger NK cells to release their cytotoxic granules
35
Q

what is the complement system?

A

a system of soluble pattern recognition receptors and effector molecules that detects and initiates the response

36
Q

what are the 3 complement system pathways?

A
  1. Clq - classical pathway
  2. mannose binding lectin and lectin pathway
  3. C3 - alternative pathway
37
Q

what is the classical pathway?

A

interacts with an antibody coated pathogen surface

38
Q

what is the lectin pathway?

A

recognises carbohydrates on pathogen surfaces

39
Q

what is the alternative pathway?

A

undergoes spontatneous hydrolysis leading to deposition of C3 convertase on pathogen

40
Q

what are the key steps of the complement amplification cascade?

A
  • circulating proteins react with each other to fight infection
  • complement proteins can be inactive precursor proteases
  • at sites of infection the complement system is activated through a triggered enzyme cascade
41
Q

how do complement proteins become activated?

A

activated by proteolytic cleavage

42
Q

what are the steps of the complement system becoming activated through a enzyme cascade at the site of infection?

A
  • active complement enzyme generated by cleavage of its zynogen precurosr
  • cleaves its substrates to active enzymatic form
  • become activated by the protease before them in the cascade
  • needs strong regulatory mechanisms to prevent uncontrolled complement activation
43
Q

how is the complement system amplified?

A

activation of a small number of complement and proteins

- hugely amplified resulting in rapid generation of a disproportionately large complement response

44
Q

what are the steps in the classical pathway?

A
  • Clq binds directly to pathogen surfaces or indirectly to antibody bound pathogens
  • this activates Clr which cleaves and activates Cls
  • Cls cleaves C4 and C2
45
Q

what are the functions of the complement system?

A
  1. opsonisation
  2. chemotaxis
  3. pathogen lysis
46
Q

what is opsonisation in the complement system?

A

enhancing phagocytosis

47
Q

what is chemotaxis in the complement system?

A

complement proteins can acts as a chemoattractant to recruit more phagocytes to the site of complement activation

48
Q

what is pathogen lysis in the complement system?

A

damage certain bacteria by creating pores in the bacterial membrane

49
Q

what is the key event in complement activation?

A
  • activation of the C3 convertase
  • whichever pathway yo will go through C3
  • in turn activates more enzymes
50
Q

what are the 4 steps of immune complex clearance?

A
  1. antibody antigen complexes are formed in the circulation
  2. complement activation leads to deposition of C3b on the immune complex
  3. complement receptor Cr1 on erythrocytes bind immune complexes through C3b
  4. erythrocytes go to the spleen and liver where phagocytosis removes immune complexes from the surface of erythrocytes
51
Q

what do innate immune cells recognise?

A

broad pathogen associated molecular patterns (PAMPs)

52
Q

how do innate immune cells recognise?

A

recognition by a small number of pattern recognition receptors (PRRs)

53
Q

what are are PAMPs?

A
  • found on nearly all members of a pathogen class
  • eg LPS of gram -ve
  • they are essential for microbial survival
54
Q

what are PRRs?

A
  • a few proteins can sense millions of pathogens
  • all cells express some PRRs
  • dendritic and macrophages express all PRRs
55
Q

what are the 4 families of PRRs?

A
  1. Toll like receptors (TLR)
  2. NOD like receptors (NLRs)
  3. C type lectin receptors (CLRs)
  4. RIG-1 like receptors (RLRs)
56
Q

what are TLRs?

A
  • localised at the plasma membrane and membranes of endosomes
  • broad range of specification
57
Q

what are NLRs?

A
  • cytoplasmic proteins

- form multiprotein complexes known as inflammasomes

58
Q

what are CLRs?

A
  • localised at plasma membrane
  • broad range specifcity
  • recognise glycans on the wall of fungi/some bacteria
59
Q

what are RLRs?

A
  • cytoplasmic proteins
  • sense viral RNA
  • signal through mitochondrial adaptor proteins
60
Q

how are PRRs activated?

A
  • pathogen
  • receptor activation
  • signalling cascade
  • transcription factor activation
  • transcription
61
Q

what is transcribed as a result of PRR activation?

A
  • amplifiers/positive feedback
  • effectors/anti-virulent
  • messengers/initiators of adaptive response
  • negative regulators of innate immunity
62
Q

what are TLR4s activated by?

A
  • LPS
  • leads to a signalling cascade
  • involves adaptor proteins
  • activation by phosphorylation of IRF3
63
Q

in TLR4 activation what is the role of IRF3?

A
  • starts transcription and production of type 1 interferons (IFN B)
64
Q

what is the role of IFN B in TLR4 activation?

A
  • IFNB is secreted through binding to its receptor
  • second wave of response (amplification)
  • dependent on STAT family transcriiption factors
65
Q

what does TLR4 depend on?

A
  • depends on where it is
66
Q

where is TLR4 localised?

A
  • only TLR localised on the membrane and the endosome
67
Q

what are important adaptors of TLR4 activation?

A

MyD88 and TRIF are important adaptors

68
Q

what does the NF-KB and AP1 pathways lead to?

A

production of inflammatory regulators

69
Q

what does the IRF pathway lead to?

A

production of type 1 interferons

70
Q

what is the NF-KB pathway?

A
  • activation downstream of PRRs lead to induction of transcription of chemokines (attract other immune cells) and cytokines (promote inflammation)
71
Q

what does IRF3 and IRF7 induce following PRR activation?

A
  • induces transcription of IFNB and IFNa (type 1 interferons)
72
Q

what is the role of type 1 interferons following PRR activation?

A
  • they are translated
  • secreted
  • bind the IFNAR
  • gives a positive feedback loop
  • get a second wave of interferon stimulated genes (SIGs) through the action of other transcription factors of the IRF and STAT families
73
Q

what are the functions of type 1 interferons?

A
  • inhibition of pathogen replication
  • induction of cell death (apoptosis) of infected and neighbouring cells
  • activation of other innate immune cells
  • activation of the antigen presentation machinery
74
Q

what is the activation of type 1 interferon pathway driven by?

A

driven by the activation of the RF family transcription factors

75
Q

what do T cells recognise?

A

recognise small linear peptides

76
Q

what can APCs process?

A

human or microbial cells to generate peptides that can be checked by T cells

77
Q

what do MHC-1 have?

A

can carry self-peptide or a microbial peptide

  • T cells recognise and kill non-self
  • non-self killed by NK cells
78
Q

what negative regulators do the innate immune gene expression programme induce?

A
  • anti-inflammatory cytokines
  • phosphatases that stop the signalling cascade
  • intracellular factors that inhibit inflammatory transcriptional factors
  • microRNAs that supress translation of inflammatory mRNAs
79
Q

what can a prolonged immune response lead to?

A

tissue damage and diseased caused by the immune system rather than the pathogen

Immunology and Infection (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions