Brainscape's Knowledge GenomeTM

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


See full index

Infection and immunity > Innate Immunity > Flashcards

Innate Immunity Flashcards

0
Q

What are the 3 primitive prevention barriers?

A 
Anatomical barriers (eg. Skin)
Chemical defences 
Commensal microflora
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What are the functions of the innate system?

A

Prevent access of pathogens
Recruit immune cells to infection site
Detect and remove pathogens
Activation of APCs

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

How does the skin protect the body? (3)

A

Epidermis is a physical barrier
Secretion of antimicrobial peptides
Fatty acids in sebum

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

How does the mucosal epithelium (eg. Gastrointestinal surface) protect the body? (2)

A

Antimicrobeles in saliva and mucus

Mucus secretion contains glycoproteins which prevent microbial adhesion

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

What is the purpose of lysosomes in bacterial defense?

A

Makes the microbes membrane accessible to antimicrobial proteins

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

What are 3 chemical defences?

A

Low pH
Bile
Pulmonary surfactant

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

How do commensal microflora help prevent pathogens? (2)

A

Compete with pathogens for attachment sites and nutrients

Support host by aiding digestion, promote maturation of immune cells

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

How many antimicrobial peptides are identified?

A

800

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

What pathogens do antimicrobial peptides work against?

A

Bacteria, fungi and viruses

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

What are antimicrobial peptides?

A

Positively charged peptides up to 60 amino acids

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

What are cytokines? (3)

A

Low MW proteins secreted by immune cells
Bind to specific cell surface receptors
Can act on self (autocrine) nearby (paracrine) or circulated (endocrine)

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

What are the four families of cytokines?

A

Hematopoietin
Interferon
Chemokine
Tumour necrosis factor

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

What do the cytokines families hematopoietin and chemokine family do?

A

Hemato: interleukins (communication between leukocytes)
Chemo: adhesion,chemotaxis and leukocyte activation

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

What do the cytokines families interferon and tumour necrosis factor do?

A

Tumour: inflammation
Interferon: anti viral

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

How are pathogens recognised by innate immunity

A

Pathogen associated molecular patterns on the pathogen are detected by pattern recognition molecules and receptors

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

What are the three types of pattern recognition molecules and receptors?

A

Soluble PR molecules
Cell membrane phagocytic receptors
Cell membrane and cytoplasmic signalling receptors

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

What is the basic principle of phagocytic PRRs (pattern recognition receptors)?

A

Cell membrane receptors stimulate ingestion of known pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are 3 mechanisms of phagocytosis?

A

Innate immune system components, eg. Neutrophils
Different types of PRR (pattern recognition receptors)
Effector mechanisms of phagocytosis

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

What are the two types Effector mechanisms?

A

Non oxidative

Oxidative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the method of non oxidative effector mechanism attack?

A

Granules with phagocytic potential merge with endosomes to form phagolysosomes

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

What is the method of oxidative effector mechanism attack?

A

Employs reactive oxygen and nitrogen species (ROS, RNS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the mechanism of oxidative phagocytosis? (4)

A

Activation of G protein coupled receptors
Activates NADPH oxidase.
Causes respiratory burst.
Causes ROSs eg. Superoxide

Activates inducible nitric oxide synthase
Causes RNS (nitric oxide)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does a respiratory burst cause cell death if ROSs are continually made?

A

Causes build up within cell of ROSs and destroy it within

23
Q

What are the 3 types of cytoplasmic signalling receptor?

A

Toll like receptors
C type lectin receptors
Nod like receptors

24
Q

What does PRR activation change within the cells gene expression? (3)

A

Causes more expression of;
antimicrobial peptides
Type I interferons
Cytokines

25
Q

What is the basic principle of toll like receptors?

A

Each receptor set detects distinct molecular pattern not present in healthy vertebrates

26
Q

What are the 5 main characteristics of neutrophils?

A 
First cells to arrive at infection site
Defend against bacteria and fungi
Act mainly via phagocytosis 
Display several types of TLR (toll like) and PRR (pattern recognition)
Contain primary and secondary granules
27
Q

What are the main characteristics of monocytes?

A

Circulate in the blood before ~8 hours before migration into tissue

28
Q

What are the 3 main characteristics of macrophages?

A

5-10x bigger than monocytes
More intracellular organelles
Can be residential or wandering

29
Q

How do residential macrophages differ from wandering?

A

Different functions and have different names, eg. Kupffer cells in liver

30
Q

What are the 4 main characteristics of dendritic cells?

A

Phagocytic APCs
Display MHC class I and II molecules
Take up pathogens by pinocytosis and receptor mediated endocytosis
On maturation migration to lymph nodes

31
Q

What are the 4 main characteristics of eosinophils?

A

Phagocytic granulocytes
Mainly located in tissues
Have effector function
Release prostaglandins (increase inflammotory response)

32
Q

What are the 2 main characteristics of basophils?

A

Nonphagocytic granulocytes

Move from blood into tissue when needed

33
Q

What are the 3 main characteristics of mast cells?

A

Differentiate only upon entering tissues
Secrete cytokines and histamine
Play role in inflammation and allergic reactions

34
Q

What are the 4 main characteristics of natural killer cells?

A

Only kill cells that are missing ‘self’ component
Contains cytotoxic granules
Express activating receptors (trigger killer cells)
Express inhibiting receptors (normal levels of MHC I molecules)

70
Q

How is NK cytotoxicity apoptosis induce apoptosis?

A

Fast dependant mechanism
Fast independent mechanism
Antibody dependant cell cytotoxicity (ADCC)

71
Q

What does ADCC stand for?

A

Antibody-dependant cell cytotoxicity

72
Q

What is the function of the complement?

A

Recognition and destruction of extracellular pathogens

73
Q

How does the complement system destroy pathogens? (4)

A

Lysis of cells
Opsonisation then phagocytosis
Triggering inflammation
Clearance of immune complexes

74
Q

What is opsonisation?

A

The process in which a antibody is marked for phagocytosis

75
Q

What are the four signs of acute inflammation?

A

Calor (Heath)
Rubor (redness)
Tumour (swelling)
Dolor (pain)

76
Q

What are the 3 roles of inflammation?

A

Recruit effector molecules to infection site
Induce local blood clotting
Initiate tissue repair

77
Q

What 2 factors initiate inflammation?

A

Tissue damage

Pathogen recognition

78
Q

What 4 blood systems activate when tissue damage inflammation occurs?

A 
Kinin system (enzyme cascade)
Clotting system (increased vascular permeability) 
Fibrinolytic system (compliment activation)
Complement (anaphylatoxins)
79
Q

What happens when pathogen activated inflammation occurs?

A

Prostaglandins and leukotrienses are released

Chemokines are released

80
Q

What do chemokines do?

A

Alter cytoskeleton and adhesiveness of target cells

81
Q

What are CAMs?

A

Cell adhesion molecules

82
Q

What are the 4 different CAM types?

A

Selectins
lg CAMs
Mucins
Integrins

83
Q

What are the roles of selectins and lg CAMs?

A

Sele: bind sialylated carbohydrates
lg: adhesion of phagocytes to endothelial

84
Q

What are the roles of mucins and integrins (cams)?

A

Mucins: bind to selectins
Integrins: bind extracellular molecules

85
Q

What are the steps involved in leukocyte extravasation (cell adhesion)?

A

Rolling freely
Activated by chemoatractant
Arrest/adhesion, mediated by integrins
Transendothelial migration (move into cell)

86
Q

what are the of TNFalpha and TGFbeta (3)

A

TNFalpha: activate macrophages and neutrophils
TGFbeta: limits inflammatory response and promotes tissue repair

87
Q

What for events take place during systematic system response to inflammation?

A

Fever
Synthesis of ACTH
production of leukocytes
Acute phase protein production

88
Q

What causes chronic inflammation?

A

Pathogens resistant to immune defences
Autoimmune diseases
Cancer

89
Q

What are the consequences of chronic inflammation? (3)

A

Continuous activation of macrophages
Fibrosis (scarring of tissue)
Granuloma (cause lesions)

90
Q

What is sepsis?

A

Spread of an infection from original site to bloodstream

91
Q

What are the consequences of sepsis?

A

Triggers blood clotting in small vessels which leads to multiple organ failure

Infection and immunity (12 decks)

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