Brainscape's Knowledge GenomeTM

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


See full index

Mpharm Y2S1 > Immunology > Flashcards

Immunology Flashcards

Exam 1

1
Q

What are the two different immune systems?

A

Innate IS
Adaptive IS

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

What is the function of the innate IS and give the cells that work in it?

A

An older system based in inflammation which everyone has the same innate immunity, which is ready to act immediately
Myeloid cells e.g. neutrophils, (other ..phil endings) lymophocytes: Natural killer cells

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

What is the function of the adaptive IS and give the cells that work in it?

A

A newer system which is based on antigen recognition, where it is acquired after time
Lymphocytes e.g B-cells and T-cells

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

What are the three main differences between the adaptive and the innate IS?

A
  1. Innate lacks memory, Adaptive has memory
  2. Innate not very specific, can identify bacteria not what type
  3. Innate has very few receptors (toll-like, mammose receptors), adaptive has unlimited T and B cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name the three main lymphocytes and which immune system they dominate in:

A

T cells- Adaptive
B cells- Adaptive
NK cells- Innate

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

Is a T-cell humoral or cellular?

A

Cellular

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

Is a B-cell humeral or cellular?

A

Humoral, so soluble

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

Which immune system can form a memory response?

A

Adaptive IS

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

What are 5 physical barriers that prevent pathogens from entering the body?

A

-Skin
-Competition of non-pathogenic bacteria
-pH, sweating decreases pH so can’t survive
-Temperature
-Host- specificity

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

What are zymogens?

A

Enzymes in the blood system which aren’t active. They need to be cleaved to become activated

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

Describe the initiation and activation steps of the complement system in the classical pathway:

A

Microbe is identified by antibody/ sugars and C1q protein detects this
C1q binds to antibody- antigen complex and becomes activated
C1q cleaves C4 into C4a+C4b
C2 binds to C4b (which is bound to the microbe) ands C1q cleaves C2 into C2a+C2b (C2b stuck to C4b)
This forms C3 convertase, this cleaves C3 which forms C3a+C3b (C3b binds to C3 convertase which forms C5 convertase)
C5 binds to C3b which C5 convertase forms C5a+C5b, C5b reunites with C6, C7, C8 and C9

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

What are the purposes of C3a and C3b in the immune response?

A

Inflammatory peptides, which leads to chemotaxis

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

What is the purpose of C3b in the immune response?

A

Binds to the surface of the microbe which helps macrophage identify bacteria, opsonization

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

What is the purpose of C5b in the immune response?

A

Reunites with C6, C7, C8 and joint with C9 together to form a pore in the bacteria which leads to destruction, cytolysis

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

How is the membrane attack complex formed?

A

C5b recruits C6, C7 and C8, they bind to the bacteria membrane and then between 8 and 16 C9 proteins comes along and form a pore in the bacterium, leading to destruction

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

Describe the initiation and activation steps of the complement system in the lectin pathway:

A

Instead of C1q, MBL binds as it can identify the mannose found on the bacteria (Mannose Binding Lectin)
Then MBL cleaves C4 to C4a +C4b (bound to microbe)
C2 binds to C4b (which is bound to the microbe) ands MBL cleaves C2 into C2a+C2b (C2b stuck to C4b)
This forms C3 convertase, this cleaves C3 which forms C3a+C3b (C3b binds to C3 convertase which forms C5 convertase)
C5 binds to C3b which C5 convertase forms C5a+C5b, C5b reunites with C6, C7, C8 and C9

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

Describe the initiation and activation steps of the complement system in the alternative pathway:

A

Proteins B,P and D bind to pathogen
C3 is bound to protein B
C3 convertase cleaves C3a+C3b
B binds to C3b to form C5 convertase into C5a +C5b

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

What are the three outcomes of the complement system?

A

Inflammation from C3a (anaphylatoxin) and C5a
Opsonization from C3b
MAC, Membrane Attack Complex, from C5b, C6, C7, C8 and C9

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

What does the C stand for in the C1q etc proteins:

A

Complement

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

How many TLRs are there?

A

Atleast 10
TLR1- TLR10

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

What do TLRs cause?

A

Production of cytokines, reactive oxygen intermediates, which causes the killing of the microbe

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

Where are Toll Like Receptors found and why?

A

Sentinel cells which are likely to have first contact with the pathogen
Macrophages, mast cells, dendritic cells

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

How can TLRs recognise pathogens?

A

Recognises pathogenic RNA/ DNA
Recognises other pathogen components e.g cell wall
TLR2- binds to bacterial lipoproteins
TLR4- binds to lipopolysaccharides
TLR5- binds to bacterial flagellum
Recognises Damage Associated Molecular Patterns (DAMPs), which are released when host cells are damaged

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

What is the name given to a cell which can divide and differentiate into any type of blood cell and where does it happen?

A

Pluripotent haematopeitic stem cell in bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the difference between 1º lymphoid tissue and 2º lymphatic tissue?

A

1º- tissue where lymphocytes are generated and mature
2º- tissue where immune responses are initiated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How many lymph nodes are there?

A

500-600

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the 3 functions of the lymph system?

A

Removal of excess fluids from body tissues
Absorption of fatty acids and transport of fat to circulatory system
Production of immune cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How does Interferon kill cells?

A

When a cell is infected it releases interferon, which spreads information to other cells
Cells can produce enzymes to kill the virus (not always)
Interferon can activate B-cells (NK Cells) which kills the infected cells
Interferon will lead to a down regulation of MHC class 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the IFN- system:

A

IFN- receptor expressed in cell surface of cells
Only become activated if IFN present
Once bound, IFN-R becomes activated and phosphorylates itself
Other proteins are phosphorylated, JAK (Janus-kinases) and STAT which causes INF- induced genes, which changes gene expression in the nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe 3 examples of Interferon induced genes:

A
  • Oligoadenylate- synthetase: polymerises ATP to 2’-5’ oligomers, so RNase (ribonuclease) L is activated, which destroys viral RNA
  • P1- Kinase: phosphorylates protein synthesis’ initiation factor elF-2 so stops translation of viral DNA/RNA
  • Mx protein: inhibits virus replication of RNA virus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How are prostaglandins released?

A

IL-1 by macrophages

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

How are prostaglandins made?

A

Phospholipids: stimulus activates phospholipase- A2 which hydrolyses phospholipids which produces arachidonicacid, this is then broken down by COX-1 (into lipoxygenases and leukotrienes) and COX-2 (into prostaglandins) enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Name 3 types of prostaglandins which cause inflammation, fever and pain:

A

Overload of PEG2, PGI2, TXA2 from COX-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are 5 symptoms of inflammation?

A

Rubor- redness
Dolour- pain, prostaglandin release
Calor- heat
Tumour- swelling
Function laesa- loss of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Describe progressive activation at the site of inflammation:

A

Due to complement activation when in infection C3a and C5a along with other chemoattractants released in blood stream on the endothelium
Polymorphonuclear leukocyte migration
Leukocyte attracted to these and attaches
Once captured they then roll on the wall slower until firm adhesion
They then transmigrate through layers of endothelium and into tissue, leads to swelling and release of prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the first stage of inflammation?

A

Vasodilation of blood vessels
This is triggered by mast cells; histamine, kinins and cytokines IL-1 and TNF-alpha
This means more blood can migrate and marginate
Diapedesis (emigration): phagocytes and other blood components force themselves between the endothelium of the blood vessels and migrate into the tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the second stage of inflammation?

A

Phagocytes are attracted via chemokine and chemotaxis
They destroy any pathogens/ mutated or dead cells
Tissue repair is then happening on damaged cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the components of neutrophile granulocytes?

A

The most common leukocyte in blood
For acute inflamed tissue
Multiple segmented nuclei (granules)
Short lifespan, 5 days
Have antibacterial enzymes e.g lysosomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the components of macrophages

A

Found in tissues and organs
Long life span, months/ years
Phagocytosis
Release cytokines/ chemokines
Recognise carbohydrate structures, PAMP = pathogen Associated Molecular Patterns (common products produced by pathogens)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are monocytes and where are they found?

A

Young macrophages, found in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Describe the steps in phagocytosis:

A

Macrophage engulfs microbe by plasma membrane, forming a phagosome (vesicle)
Lysosome attaches and forms a phagolysosome and digests the microbe
Anything indigested is released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are NK cells and what is one way how they work?

A

Natural killer cells
Kills an infected cell by identifying the cell and killing it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is another way in how an NK cell can kill an infected cell?

A

NK cell attaches to the macrophage with microbe inside of it
Macrophage releases IL-12, which binds to the NK receptor which releases cytokine IFN-gamma
This helps the macrophage kill the bacteria and not itself

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What two receptors do NK cells have?

A

Activating and Inhibitory receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Why is there no MHC class 1 when viruses are present?

A

MHC class 1 is a protein and viruses stop protein production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Where does each receptor of an NK cell bind to in a normal cell?

A

Both receptors bind
Inhibitory receptor binds to MHC class 1 protein found on all human cells apart from RBC’s
This binding allows the survival of the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How does the inhibitory cell binding in an NK cell to a normal cell stop the killing of it?

A

Binding produces phosphotase which removes phosphate from tyrosine kinases which normally causes the killing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How to NK cells kill viruses?

A

Viruses don’t normally have the MHC class 1 on them so won’t be able to have the essential binding of the inhibitory receptor and therefor will kill the virus by shutting down the activating receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What does MHC stand for and give another name for it:

A

Major Histocompatability Complex
Also be called HLA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Where is MHC class 1 protein found?

A

On all cells, marker for all cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Where is MHC class 2 protein found?

A

On macrophages, B- cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the function of MHC 1?

A

Helps activate only CD8 positive T-cells find antigens and present them on T- cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the function of MHC 2?

A

Helps activate only CD4 positive T-cells, find antigens and present them on T-cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Where are T-cells able to bind?

A

ONLY things presented in MHC complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What do B-lymphocytes do?

A

Block infections and eliminate extracellular microbes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What do T-helper lymphocytes do?

A

Activate macrophages to kill phagocytosed microbes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What do T-cytolytic lymphocytes do?

A

Kills infected cells and illuminate reservoirs of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Describe one way an antigen is captured and presented by a T-cell:

A

Microbe will be present on the skin
Dendritic cells capture the microbe and moves to lymph nodes which there lots of B and T cells will present antigen towards the T-cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Describe another way an antigen is captured and presented by a T-cell:

A

Antigen enters the blood stream and into the spleen, which in there the antigen capturing cells eat the pathogen, forms an MHC complex and presents it on surface for T-cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the functions of immature dendritic cells and where are they found?

A

Found in the epidermis
They are good at hoovering antigens by makropinocytosis or phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the functions of mature dendritic cells and where are they found?

A

When migrate to the lymph (via lymphatic vessels) and spleen they mature
Good at MHC expression and B7 expression
Good at adhesion molecules
Good at expression to naive T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

How does a Class 2 MHC allow the pathway of intracellular processing of a pathogen?

A

Endocytosis of an extracellular microbe occurs and an endocytic vesicle forms
Class 2 MHC forms in the ER and MHC forms a vesicle and fuses with the endocytic vesicle and displayed on the surface of the cell ready to engage with a CD4+ T-cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

How does a Class 1 MHC allow the pathway of intracellular processing of a pathogen?

A

The microbe is present in the cytosol
The microbial protein unfolds and peptides present in cytosol
Class 1 MHC forms in the ER and binds to peptides in cytosol
MHC- peptide complex is transported to cell surface and presented to CD8+ T-cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are the differences between an MHC class 1 pathway of intracellular processing and MHC class 2?

A

In 1, the microbe is present in the cytosol
In 2 the microbe is outside the cell and is moved in by phagocytosis and in a vesicle in the cytosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Where are T-cells produced?

A

Bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Where do T-cells mature and then where do they go after?

A

Mature in the Thymus and then into secondary lymphatic organs, blood, spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

How are T-cells developed?

A

From thymocytes, a and B TCR recombination occurs
Beta recom= CD4- and CD8-
Alpha recon= CD4+ and CD8+
Positive and negative selection occurs with TCR+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How are T-cells chosen in positive and negative selection?

A

If weak (good) bond with MHC II, then CD4+, if weak (good) bond with MHC I, then CD8+, positive selection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Why is a weak bond with T-cells and MHC better than a strong bond?

A

A strong bond leads to activation without antigen and leads to damage, negative selection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What type of T-cells are CD4+?

A

Helper cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What type of T-cells are CD8+?

A

Cytotoxic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

How is a T-cell replicated from an antigen-presenting cell (APC)?

A

Induction phase
Naive CDX+ ( CD8/4) binds to APC, with co-signal of CD28- CD80/86 and becomes activated
It releases cytokine IL-2, which binds to cytokine IL2 receptor and leads to clonal expansion
Differentation occurs when the T-cell is made into an effector cell or memory cell

73
Q

Can a naive T-cell become activated by just binding to the APC and why?

A

No, needs a co-signal of CD28 – CD80/CD86 which helps with signal transduction

74
Q

What two proteins are needed for adhesion and stabilisation of a T-cell stimulation?

A

LFA-1 and ICAM1

75
Q

What are the proteins that help with signal transduction of T- cell stimulation?

A

CD28- CD80/86
CD3 and ITAM

76
Q

What is required for a T-cell interaction can activate?

A

At least 3 t-cell receptor interactions

77
Q

What are the two T-helper cells called?

A

Th1 and Th2

78
Q

What is the Th1 cytokine useful for?

A

Fighting intracellular pathogens

79
Q

What are the two products of Th1 cells?

A

Interferon gamma
Tumour- Necrosis- Factor (TNF)

80
Q

What is the purpose of interferon gamma?

A

Th1 marker cytokine
Macrophages: activation and MHC up regulation
Elimination of intracellular bacteria
Antiviral function

81
Q

What is the purpose of TNF?

A

Macrophages: activation, NO production
Elimination of intracellular bacteria
Dendritic cells: maturation, migration

82
Q

What causes T- helper cells to differentiate into Th1 and Th2?

A

Th1= IL-12
Th2= IL-4

83
Q

What is the main purpose of Th1 cells?

A

Activate macrophages

84
Q

What is the induction phase of Th1 helper T-cells?

A

IL-12 released from macrophage with bacteria
Dendritic cells take up bacterial protein
IL–12 helps with differentiation of t cells into helper T cells (Th1)

85
Q

What is the effector phase of Th1 helper T-cells?

A

INF- gamma leads to activation and increased MHC
TNF- NO production
Lymphotoxin- lysis of infected cells
IL-3/ GM- CSF- production/ differentiation

86
Q

What is the main purpose of Th2 cells?

A

Activate B-cells

87
Q

What are Th2 T-helper cells useful for?

A

Important for antibody answer and allergic reactions

88
Q

What are the three products of Th2 cells?

A

IL-4
IL-5
IL-10

89
Q

What is the purpose of IL-4?

A

Th2 marker cytokine
Activation/ growth of B-cells
Essential for IgE, Th2 development
Positive feedback, more IL-4, more Th2

90
Q

What is the purpose of IL-5?

A

B – cell differentiation, IgA synthesis
Growth/differentiation of eosinophils

91
Q

What is the purpose of IL-10?

A

Regulatory cytokine
Inhibitor of macrophage function, as when Th2, want to rely on antibodies and not macrophages

92
Q

How are naive cytotoxic T-cells activated?

A

Antigen presentation plus stimulation of naive CD8 cells- needs co-stimuation of CD28
Proliferation/ clonal notification using IL–12, differentiation with help of CD4 cells
Effect CD8 T-cell kills target

93
Q

Describe the non-secretory mechanism of how a cytotoxic T-cell works:

A

Target has Fas receptor on cell surface, and cytotoxic T–cell has its ligand
When bound and activated, signal for target cell to undergo apoptosis
Binding of TCR and MHC still occurs

94
Q

What is a Fas receptor?

A

A death receptor

95
Q

Describe the secretory mechanism of how a cytotoxic T cell works:

A

Cytotoxic T cell can release perforin granzyme which makes holes in target cell and kills it
Binding of TCR and MHC still occurs

96
Q

Why is the secretory mechanism unfavoured?

A

It causes the release of the cell into the tissue
This infected tissue can release enzymes which could be digestive for eg and damage surrounding cells

97
Q

What part of the antibody has the antigen binding site?

A

The variable heavy chain and variable light chain

98
Q

Why is the conserved heavy chain of an Ab important?

A

This heavy chain is different for different classes of antibodies

99
Q

How many classes of antibodies are there?

A

Five

100
Q

How do antibodies neutralise a microbe?

A

They can bind to the microbes and blocks from infecting the cell so prevent microbe from binding to the receptor

101
Q

Name the five types of antibodies:

A

IgA, IgG, IgE, IgD, IgM

102
Q

What is the anti body involved in first primary response?

A

IgM

103
Q

What is the antibody involved in the secondary response?

A

IgG

104
Q

What are the different fragments in the variable region?

A

V, D, J,

105
Q

What is junctional diversity?

A

Adding or subtracting nucleotides as this changes the protein sequence which creates more diversity in antibodies

106
Q

What is the name given for production of the variable region on the heavy chain and how is this done?

A

Somatic recombination
D – J chosen ones joining in B-cell clone
Splicing removed the things in between
V – DJ joining and same thing happens again
Then transcription, RNA processing, variable region is produced, then add constant region

107
Q

What is the production for the variable region of the light chain?

A

The same as for the heavy chain but the D segment isn’t involved

108
Q

What is somatic hyper mutation and name three ways this is done:

A

Different ways antibody changed once displayed:
1. Affinity maturation
2. Switch from membrane to secreted form
3. Isotype switching

109
Q

What is affinity maturation?

A

Small mutation over time inside the antibody which should increase the affinity and make a better antibody

110
Q

What is switching from membrane to secreted form?

A

The antibody is released to the blood stream so it can find antigens and bind to them

111
Q

What is isotope switching?

A

Replace constant region of the antibody (heavy chain) so changes class of Ab

112
Q

Where are B cells made and how do they mature?

A

Made from stem cells in bone marrow and will mature there
Pro-B - no Ab on cell surface
Pre-B - recombined H chain Ab not completely formed+ displayed
Immature B- IgM only formed and displayed as light chain recombined
Mature B- IgM and IgD formed so can leave bone marrow

113
Q

How do B cells undergo isotope switching?

A

Have switch regions which recombination can occur by looping out

114
Q

Describe the primary antibody response:

A

Naive B cell- activated
Ab secreting cells release IgM, some IgG formed
After, low levels of IgG and plasma cells around

115
Q

Describe the repeat infection response of an antibody:

A

More antibody produced and faster as already have higher base levels of B cells
IgG Ab acting which have a higher affinity for pathogen as its very specific, better than IgM, so then base level of memory B cells higher than before

116
Q

What are three characteristics of memory B cells?

A

Only secretion of IgA, IgG and IgE
Enhanced Ab affinity compared to naive
Increased somatic hypermutation

117
Q

What are three characteristics of memory T cells?

A

Need the same minimal antigen conc as naive T cells
Cytokine secretion less than 3 hours after antigen contact
Development of cytotoxicolical activity 12 hours after activation- really quick

118
Q

What is an allergy?

A

And unwanted inflammatory and immune response

119
Q

Name and describe predisposing factors which favours atopic phenotypes:

A

Genetic- certain MHC II genes
- certain Th2 cytokine genes
- Pro- inflammatory response genes
Environmental- Excessive hygiene
- Having few siblings
- Decreased exposure to farm antigens
Triggering events- Hormonal fluctuation
-Emotional distress
- Nutritional deficit

120
Q

State and describe the types of hypersensitivity reactions:

A

Type one: immediate anaphylactic hypersensitivity (IgE)
Type two: antibody-dependent cytotoxic hypersensitivity (IgG, IgM) -triggers complement (NK cells)
Type three: complex mediated (IgG, IgM)
Type four: cell mediated hypersensitivity (depends on T-cell)

121
Q

What is an important mast cell growth factor? Type 1

A

Stem cell factor (SCF)

122
Q

Where are mast cells differentiated and found? Type 1

A

Differentiation in tissue
Found in connective tissue

123
Q

What receptors do mast cells contain for IgE? Type 1

A

FcERI

124
Q

Why are mast cells important in the innate immune system? Type 1

A

– Can get a specific effect to cells to potential sites of infections
– Enhance flow of lymph fluid to lymph nodes
– Induces muscle contraction which forces pathogen out of lung/gut
– Important against defence of worm infections

125
Q

Whats the initiation of a type 1 immune response?

A

An allergen is detected by an immature T cell and creates a TH2 cell
B cell displays the IgM antibody and also the IgE which triggers an immune response

126
Q

How does IgE trigger a type 1 allergic reaction?

A

IgE binds to mast cells, as mast cells have a lot of IgE receptors
Repeat exposure to the allergen will cause an allergic reaction
The allergen binds to antibody on mast cell which activates it and causes degranulation
Mast cells have different effects depending on location

127
Q

What is degranulation?

A

Granules in mast cells, containing histamines, are released which leads to an immediate hypersensitivity reaction

128
Q

What happens when mast cells are activated in the GI tract?

A

An increase in fluid secretion therefore expulsion of GI contents E.G. diarrhoea/vomiting

129
Q

What is a late phase reaction in type one hypersensitivity?

A

4 to 16 hours after being exposed to the allergen a less significant reaction occurs

130
Q

Describe anaphylactic shock: Type1

A

After initial exposure to toxin, persons immune system become sensitised
Tissues in different parts of the body release histamine and other substances
The airways, GI tract and blood vessels all being affected by histamine
These affects result in shock, fluid can leak into the alveoli of the lungs causing pulmonary Adema

131
Q

What is the treatment for anaphylactic shock? Type 1

A

Epinephrine by injection immediately, it opens airways and increases BP
Then intravenous fluids and meds to support actions of heart
Then antihistamines and corticosteroids

132
Q

What are the complications of an anaphylactic shock? Type 1

A

Heart arrhythmias, shock, cardiac arrest, airway obstruction

133
Q

Give an example of type II hypersensitivity and what occurs during it?

A

E.G.blood transfusion wrong type of blood
Target cells become coated with antibodies, leads to cell destruction by phagocytosis in liver or spleen, antibody-dependent cellular cytotoxicity which causes hypersensitivity reaction

134
Q

Give an example of type III hypersensitivity and what occurs during it?

A

E.G.malaria or hepatitis
Immune complexes aren’t cleared from blood
Antibodies bind to soluble antigens in blood which often become lodged/ precipitate in narrow channels in body and provoke immune response damaging surrounding cells such as increased vessel permeability and lots of cells migrating to the tissue
e.g mast cells stim by C3a to release mediators- serum sickness which occurs when antigen persists in blood after sensitisation
Neutrophils stim by C5a to secrete enzymes and toxic oxygen species

135
Q

Give an example of type IV hypersensitivity and when does it occur?

A

E.G. contact dermatitis
Occurs 24-48 hours after, also called delayed-type hypersensitivity

136
Q

What is the difference between type IV hypersensitivity and all the other hypersensitivities?

A

It’s a T-cell mediated and not antibody-mediated

137
Q

What occurs during type IV hypersensitivity?

A

APC’s takes up the antigen and presents to T cells
Requires prying antigen-specific T cells
Localise inflammatory response, kill cells exposed to antigen, lots of cells migrate to the site

138
Q

What test can be used to determine a Type IV hypersensitivity and give an example:

A

Mantoux test- test whether allergic or not
Tuberculin skin test- injecting a small amount of substance into forearm

139
Q

Which histamine receptor is found on the smooth muscles and what is the effect of histamine on them?

A

H1, from the constriction, contraction of GI tract

140
Q

Which histamine receptor is found on the endothelium and what is the effect of histamine on them?

A

H1, vasodilation, increasing capillary permeability which leads to oedema

141
Q

Which histamine receptor is found on the sensory nerve endings and what is the effect of histamine on them?

A

H1, pain and itching

142
Q

Which histamine receptor is found on smooth muscles of the blood vessel and what is the effect of histamine?

A

H2, vasodilation

143
Q

Which histamine receptor is found on immune active cells and what is the effect of histamine?

A

H4, chemotaxis

144
Q

What are three things that can reduce the effects of released histamines?

A
  1. Physiological antagonists
  2. Histamine release inhibitors
  3. Histamine receptor antagonists/antihistamines
145
Q

How do physiological antagonist work against histamines?

A

e.g. epinephrine
Smooth-muscle actions opposing histamine but acts on different types of receptors, not histamine receptors

146
Q

Name two histamine release inhibitors:

A

a) Mast cell stabilisers
b) Beta 2 adrenergic agonists

147
Q

What are first-generation antihistamines and how do they work?

A

Sedating, lipophilic compounds that readily cross blood brain barrier
Rapidly absorbed from GI tract, widely distributed, duration of action for 4 to 6 hours as extensive metabolised by the cytochrome P4 50 metabolite active and excreted by kidney

148
Q

What are second generation antihistamines and how do they work?

A

Nonsedating, poorly penetrate the blood brain barrier
Rapidly absorbed by the GI tract, widely distributed
Elimination – cetrizine, urine
– Fexofenadine, bile

149
Q

Which type of antihistamines have an anticholinergic affect and what does this mean?

A

First generation, inhibit responses to Ach that are mediated by muscarinic receptors
Effects are dry mouth, blurred vision, constipation

150
Q

Which type of antihistamine has an effect on the CNS and how does it do this?

A

First generation, as it produces a CNS depression which manifests sedation, which can also prevent motion sickness
Excitation may occur in children rather than sedation
Second generation has no effect on CNS as can’t cross the blood brain barrier

151
Q

Give three drug interactions with with first-generation H1 antihistamines:

A

– Co-administering with cytochrome P450 inducers will decrease activity
– co-administering P450 inhibitorsE.G antifungals will increase activity
– Additive CNS depression with:
opioids, sedatives, narcotics, alcohol

152
Q

Give three examples of second-generation histamine receptor antagonists:

A

Fexofenadine, loratadine, cetirizine

153
Q

Give two examples of mast cell stabilisers and how are they used?

A

Cromolyn and Nedocromyl
Not orally absorbed, so given as a powder by inhalation
Inhibit histamine release by inhibiting chloride channels on mast cells

154
Q

What are mast cell stabilisers used for and give side-effects:

A

Against bronchial asthma and allergic rhinitis
SE = dry mouth, throat irritation, cough/wheeze

155
Q

Which immune system is the complement system in even though it has antibodies involved?

A

Innate

156
Q

What is the difference in specificity between the innate and adaptive IS?

A

Innate- can identify classes of microbes and for different microbes the same receptor
Less specific than the adaptive immune system which has distinct antibodies for distinct microbes

157
Q

What is the difference in receptors between the innate and adaptive IS?

A

Very few receptors in innate e.g mannose, toll like and N-formyl methionyl
In adaptive there is somatic recombination so greater diversity

158
Q

Describe the structure of T cell receptors:

A

Composed of alpha and beta chains
Consists of a conserved and variable region
The variable region binds to the antigen
TCRs only recognise antigens when presented by MHCs

159
Q

Which cells express MHC class 1?

A

On all cells with a nucleus
High expression on lymphocytes
Low expression on non lymphoid cells

160
Q

Which cells express MHC class 2?

A

Not on all cells
High expression on antigen presenting cells e.g dendritic, macrophages and B cells
Activated T cells

161
Q

Where does MHC class bind to?

A

Only stable on cell surface with peptide

162
Q

Where are immature dendritic cells found?

A

Epidermis

163
Q

Where are mature dendritic cells found?

A

T cell rich areas like lymph nodes and spleen

164
Q

Why is somatic recombination called that?

A

Somatic as happens in B cells

165
Q

State 4 ways in which antibody diversity is reached:

A

Combination of gene segments
Junctional diversity
Combination of different heavy/ light chains
Somatic hypermutation

166
Q

Describe the difference in reactions when exposed to an antigen in the different ISs:

A

In adaptive:
IgM conc increases initially, then IgG conc increases, with immune response getting better over time
In innate:
Response is the same each time

167
Q

What is an allergen?

A

A substance that is recognised by the immune system and cause an allergic reaction

168
Q

What is an allergen?

A

A substance that is recognised by the immune system and cause an allergic reaction

169
Q

State what happens in a type 1 hypersensitivity reaction and what are the symptoms because of it:

A

Dilation of BV- causes local redness, if dilation is widespread it can contribute to decrease vascular resistance so decrease in BP so shock
Increased capillary permeability- swelling
Constriction of bronchial airways- wheezing and difficulty breathing
Stem of nerve endings- itching and pain in the skin

170
Q

What characteristics do allergens have that favours a Th2 response?

A

Proteins
Active enzymes- proteases
Low dosage
Low molecular weight as can diffuse into mucosa
Good solubility

171
Q

Name and describe products which can be released by activated mast cells:

A

Enzymes- change in connective tissue mass
HISTAMINE- increased permeability, contracts muscle, toxic for parasites
Chemotactic factors- attract neutrophils/ eosinophils
Cytokines- Th2 response, inflammation
Various mediators

172
Q

What is atopy?

A

The genetic predisposition to make IgE antibodies in response to allergen exposure patients prone to IgE mediated allergic reactions are said to be atopic

173
Q

State people more prone to allergen exposure:

A

Males
Small familes
Prenatal diet and smoking

174
Q

What is the atopy phenotype:

A

Genes on chromosomes 5 and 11

175
Q

Describe the lymph system:

A

Network of lymphoid organs
1º- lymphoid tissue, where lymphocytes are generated and mature, e.g bone marrow
2º- lymphatic tissue, where immune responses are initiated, e.g spleen, lymph nodes

176
Q

What does the spleen do?

A

Collects antigens from the blood stream

177
Q

How does ibuprofen and aspirin work?

A

Inhibits COX 1 and 2

178
Q

What type of receptors do macrophages have on them and how many different kinds are there?

A

Toll like receptors
At least 10

179
Q

What other receptors do macrophages have and how do they work?

A

Have GPCR’s which bind to other chemokine which cause macrophages to migrate into tissue, to site where bacterial infection is

Mpharm Y2S1 (12 decks)

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