Innate Immunity Flashcards
1
Q
What are the 3 types of immune responses?
A
- ) Innate Immunity
- ) Adaptive Immunity
- ) Passive Immunity
2
Q
What does passive immunity provide?
A
Immediate short-term immunity (under a year)
3
Q
How is passive immunity acquired?
A
From other individuals from the transfer of antibodies
4
Q
What are the two types of antibodies?
A
Natural Maternal and Artificial Antibodies
5
Q
In what part of the blood are antibodies localized?
A
Plasma
6
Q
How long do antibodies last?
A
Up to 10 months - a year
7
Q
Why do patients who require antibodies need to go for reoccurring treatments?
A
Antibodies don’t last forever, so every 6-10 months a retreatment is required
8
Q
What is one main source from where we get natural antibodies?
A
Our mothers via birth
9
Q
What types of immunity are present in a newborn?
A
Passive & Innate (Adaptive not yet developed)
10
Q
How are maternal antibodies transferred to a newborn?
A
Done in utero - antibodies cross through the placenta to the baby which allows them to be born with passive immunity
11
Q
What additional way can maternal antibodies be passed to a newborn?
A
Through breastfeeding
12
Q
Innate immunity is…
A
The first line of defence against a pathogen
13
Q
What is innate immunity most effective at?
A
Stopping majority of pathogens at an EARLY stage
14
Q
From who is innate immunity inherited from?
A
Our parents allow us to be born with innate defenses
15
Q
Do all humans vary with their innate defences?
A
NO! All humans have the same defences
16
Q
How does innate immunity respond when a pathogen contacts the body?
A
The defences are immediately initiated
17
Q
How does innate immunity respond to a pathogen who has previously attacked the same person (repeated pathogen exposure)?
A
The innate immune system has NO MEMORY and thus responds the same for every exposure. This immune response is non-adaptive
18
Q
Immune Barrier
A
Blocks a pathogen from entering into the tissues
19
Q
What happens if the innate immune system is unsuccessful?
A
Adaptive immune system will become active to eliminate the pathogen
20
Q
4 modes of pathogen entry into the body:
A
- ) Skin (wound)
- ) Gastrointestinal Tract (ingestion)
- ) Respiratory Tract (breathing)
- ) Reproductive
21
Q
What is the physical barrier that prevents pathogen entry?
A
Epithelial cells
22
Q
What are the 4 properties of epithelial cells?
A
- ) From tight junctions
- ) Rapidly renewable
- ) Desquamation (shedding) of epithelium, which removes pathogens with the cells
- ) Secrete antimicrobial peptides (defensins)
23
Q
Why are tight junctions located between epithelial cells?
A
To prevent pathogens from moving into the tissue
24
Q
What are defences?
A
Defences are pore-forming antimicrobial peptides
25
What is the role of defensins?
To kill bacteria, viruses and fungi
26
Forming a pore in the cell membrane causes what to happen?
An efflux of nutrients and essential ions as well as influx of water from the extracellular environment
27
Mechanical Barriers
Expelling or flushing out pathogens
28
Chemical Barriers
Fatty acids, enzymes, etc.
29
Microbiological Barriers
Normal flora compete for nutrients and attachment to epithelium
30
Where is the microbiota found?
Anywhere where there are epitheliala cells lining an entry point. Mouth, respiratory tract, gastrointestinal tract, genital, skin.
31
How large in comparison to our body weight is the microbiota?
10% of our weight
32
Where is the microbiota MOST COMMONLY found?
Lower intestine & mouth
33
How does our microbiota benefit us?
Nutritional and digestive benefits. Also provides immune protection (barrier)
34
Can the microbiota be harmful to us?
No, but it requires nutrients to survive and can cause infections called "opportunistic pathogens"
35
What is an "opportunistic
| pathogen?
Something that can become pathogenic when opportunity arises
36
Why can antibiotics not be good for our health?
Antibiotics kill both pathogenic bacteria and beneficial bacteria because it can't distinguish between the two
37
Ingesting more drugs then necessary causes what?
Destroys our microbiota and our good bacteria which is breaking down our barrier. This leaves us more susceptible to infection
38
What are the 4 types of barriers that epithelial cell provide?
Physical, Mechanical, Microbiological, Chemical
39
Extracellular Pathogen
Pathogen resides outside the house cell. Primarily bacteria.
40
Intracellular Pathogen
Pathogen resides inside the host cell. Primarily viruses.
41
True or False: Many pathogens have both an extracellular and intracellular phase.
True. Viral entry into host cell involves the transition form the extracellular to the intracellular space
42
What are the two main cells of innate immunity?
Phagocytes and Lymphoctyes
43
What are the types of phagocytes?
Neutrophils, Macrophages, Immature Dendritic Cells
44
What are the types of lymphocytes?
Natural Killer Cells
45
What do phagocytes destroy?
Extracellular pathogens by phagocytosis
46
What do lymphocytes kill?
Intracellular pathogens by apoptosis
47
List the 3 steps in phagocytosis
1. ) Phagocyte binds a pathogen which triggers phagocytosis
2. ) Cell membrane extends around microbe and internalizes it into a phagosome
3. ) Phagosome fuses with lysosome containing anti-microbial mediators (= phagolysosome) which KILLS THE PATHOGEN!
48
Where does the killing of a bacterium occur during phagocytosis?
In the phagolysosome. This allows us to keep the phagocyte safe
49
How does the lysosome kill the pathogen?
Lysosome contains acids and enzymes that quickly kill the pathogen
50
What enzymes are found in the phagolysosome?
1. ) Defensins, Lysozyme - damage pathogen cell wall
2. ) NADPH oxidase - produce toxic oxygen metabolites
3. ) Nitric oxide synthetase - produce toxic nitric oxide
51
How do phagocytes bind extracellular pathogens?
Using PRRs - Pattern Recognition Receptors
52
Where are PRRs expressed?
On the surface or inside phagocytes?
53
How do PRRs bind to exclusive pathogens?
They bind to PAMP - Pathogen Associated Molecular Pattern
54
What express PAMPs?
Pathogens only!
55
When are PAMPs expressed?
Always
56
Why are there a limited number of PRRs?
PRRs can bind to multiple PAMPs and thus less PRRs are necessary
57
How many PRRs are there?
Less then 100
58
Why do PRRs only recognize and bind to pathogens?
- Allows efficient recognition of pathogens? (little mutations)
- Very effective at destroying pathogens at an early stage of infection
59
Where are neutrophils found?
In the blood, but most abundant in white blood cells (leukocytes)
60
How do neutrophils get to the infected tissue?
By circulating through the blood and rapidly entering into the infected tissues
61
How many neutrophils are produced a day?
100 billion
62
If we took a count of neutrophils from our blood what would be expect to see in a sick patient?
An increase in neutrophil count usually by twice as much (100 billion in healthy, 200 billion in sick)
63
Why are neutrophils short lived?
Limited room in the blood stream
64
What occurs in a patient with neutropenia?
Low neutrophil count. under 500/uL -> Normal is 1500/uL
65
Where are macrophages located?
In tissues
66
How do phagocytes arise?
From blood monocytes that have migrated into tissues
67
What key role do macrophages play in adaptive immunity?
Initiate adaptive immunity
68
Where are immature dendritic cells located?
In circulating blood and in tissue near epithelial cells
69
Why are IDC located where they are?
Allows for quickly starting of phagocytosis
70
How do immature DC differ from mature DC?
Immature DC play a role in innate immunity while mature DC initiates adaptive immunity
71
What types of immune cells reside in the tissue?
DC & Macrophages
72
What types of immune cell reside in the blood surrounding infected tissues?
Neutrophils, DC & Monocytes
73
Natural Killer Cells
A type of lymphocyte that circulates in the blood
74
What is the function of a Natural Killer Cell
To kill INTRAcellular pathogens (viruses) as well as cancer cells
75
How is a natural killer cell activated?
By the binding of NK cell to a infected cell
76
What happens when a NK cell is bound to an infected cell?
Perforin and granzyme are released onto the infected cell causing APOPTOSIS
77
Perforin
Forms a pore in infected cell membrane which allows granzyme to enter the virus-infected cell
78
Granzyme
Degrades DNA/RNA
79
What do NK cells fail to do?
Eradicate INTRACELLULAR BACTERIA!
80
Intracellular bacteria
Bacteria that survive/replicate inside a phagocyte
81
How do intracellular bacteria bypass phagocytosis?
They inhibit fusion or resistance to lysosomal contents and begins to replicate in the phagosome. The bacteria will then escape the phagosome and replicate again in the cytoplasm
82
What are the two types of soluble molecules?
1. ) Cytokines
| 2. ) Acute-Phase Proteins (complement protein 3)
83
Cytokines
Small proteins secreted by ACTIVATED nucleated cells
84
Cytokines are responsible for...
Communication with other cells as well as within itself
85
Cytokines can control or suppress..
Cell behaviours including proliferation, growth, maturation and survival
86
Cytokines play a role in what immunities?
Both innate & adapative
87
How does a cytokine relay information?
Cytokine binds to a receptor on the cell surface which relays a signal to the cell on how to behave
88
6 Types of cytokines
Chemokines, Interferon (IFN), Pro-Inflammatory Cytokines, Anti-Inflammatory Cytokines, Growth Factors, Colony Stimulating Factors (CSF)
89
Which types of cytokines play a key role in innate immunity?
Chemokines, Interferon, Pro-Inflammatory Cytokines
90
Which types of cytokines play a key role in hematopoiesis?
Anti-Inflammatory Cytokines, Growth Factors, Colongy Stimulating Factors
91
How is haematopoiesis regulated?
By cytokines
92
Haematopoietic Stem cells diverge into...
Lymphoid Stem Cells and Myeloid Stem Cells
93
Lymphoid Stem Cells diverge into
B-cells, T-cells and NK cells
94
Myeloid Stem Cells diverge into
Neutrophils and others including Dendritic Cells and Macrophages
95
What do activated cells secrete?
Many different types of cytokines simultaneously
96
What does PRR-PAMP binding by phagocyte result in?
Phagocytosis (death of pathogen) and Cytokine Production (pro-inflammatory cytokines and chemokines)
97
What do TNF, IL-1, and IL-6 all do?
Activate endothelial cells
98
What do activated endothelial cells do?
Vasodilate - increase blood flow, and increase blood vessel permeability. This allows circulating immune cells + soluble molecules to enter into infected tissue
99
Chemokines
Chemoattractant cytokines. Function is to attract immune cells
100
What are the key components of inflammation?
Phagocytosis & cytokines
101
What causes pain during an infection?
The release of mediators from a phagocyte
102
What causes redness, heat and swelling?
Vasodilation and increased vascular permeability
103
How is a fever started?
Infected tissue -> Activated phagocyte -> Cytokines enter circulation -> Activate hypothalamus -> Produce Prostaglandins -> Fever
104
What does a fever indicate?
A fever indicase an infection. It is an early innate response.
105
What do fevers help in?
Killing a pathogen. High temperatures make it hard for a pathogen to replicate and survive
106
How is inflammation started?
Infected tissue -> Activated phagocyte -> Cytokines enter circulation -> Activate hepatocytes -> Secrete acute phase proteins -> Enter circulation -> Enter infected tissue
107
When the liver absorbs cytokines, what is produced?
Complement protein 3
108
What can some APP act as?
Soluble PRRs which bind to PAMPs on extracellular pathogen
109
Opsonin
A molecule that "marks" a pathogen for destruction by phagocytosis
110
How does opsonization occur?
APP binds to receptor on pathogen and enters the pathogen. APP tigers phagocytosis.
111
What happens to C3 (Complement Protein 3) when in the presence of a pathogen?
Cleaves into C3a + C3b
112
What does C3b do, that C3a does not?
C3b binds to its receptor on the phagocyte, while C3a simply recruits phagocytes
113
What receptors on phagocytes bind extracellular pathogens and trigger phagocytosis?
Surface PRRs and Acute-Phase Protein Receptors
114
What are the two roles of C3a that help in maintaining inflammation?
1. ) Activates endothelial cells - increase vascular permeability
2. ) Attracts blood leukocytes to the site of infection
115
Why is inflammation beneficial?
It recruits circulating cells & soluble plasma molecules required for hot immune defines into infected tissue
116
What are the two important antivirals?
Type I Interferons - IFN-alpha and IFN-beta
117
Where is PRR located?
Inside cells
118
How does PRR inhibit viral replication?
By binding to viral nucleic acid - PAMP.
119
What does IFN do?
Tells natural killer cell to kill infected cell
120
When are Type I IFNs secreted?
Very early after a viral infection
121
How do Type I IFNs effect healthy cells?
Induce antiviral enzyme production to protect themselves from viral infection... Limits viral spread
122
What viral infections can be treated with Type I IFNs?
Herpes, Viral Hep B, Hep C
123
What happens if a virus block IFN production by the infected cell?
Our immune system relies then on T cell immunity
