Immunology Flashcards
Exam 1
1
Q
What are the two different immune systems?
A
Innate IS
Adaptive IS
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
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
4
Q
What are the three main differences between the adaptive and the innate IS?
A
- Innate lacks memory, Adaptive has memory
- Innate not very specific, can identify bacteria not what type
- Innate has very few receptors (toll-like, mammose receptors), adaptive has unlimited T and B cells
5
Q
Name the three main lymphocytes and which immune system they dominate in:
A
T cells- Adaptive
B cells- Adaptive
NK cells- Innate
6
Q
Is a T-cell humoral or cellular?
A
Cellular
7
Q
Is a B-cell humeral or cellular?
A
Humoral, so soluble
8
Q
Which immune system can form a memory response?
A
Adaptive IS
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
10
Q
What are zymogens?
A
Enzymes in the blood system which aren’t active. They need to be cleaved to become activated
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
12
Q
What are the purposes of C3a and C3b in the immune response?
A
Inflammatory peptides, which leads to chemotaxis
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
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
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
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
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
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
19
Q
What does the C stand for in the C1q etc proteins:
A
Complement
20
Q
How many TLRs are there?
A
Atleast 10
TLR1- TLR10
21
Q
What do TLRs cause?
A
Production of cytokines, reactive oxygen intermediates, which causes the killing of the microbe
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
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
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
25
What is the difference between 1º lymphoid tissue and 2º lymphatic tissue?
1º- tissue where lymphocytes are generated and mature
2º- tissue where immune responses are initiated
26
How many lymph nodes are there?
500-600
27
What are the 3 functions of the lymph system?
Removal of excess fluids from body tissues
Absorption of fatty acids and transport of fat to circulatory system
Production of immune cells
28
How does Interferon kill cells?
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
29
Describe the IFN- system:
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
30
Describe 3 examples of Interferon induced genes:
- 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
31
How are prostaglandins released?
IL-1 by macrophages
32
How are prostaglandins made?
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
33
Name 3 types of prostaglandins which cause inflammation, fever and pain:
Overload of PEG2, PGI2, TXA2 from COX-2
34
What are 5 symptoms of inflammation?
Rubor- redness
Dolour- pain, prostaglandin release
Calor- heat
Tumour- swelling
Function laesa- loss of function
35
Describe progressive activation at the site of inflammation:
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
36
What is the first stage of inflammation?
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
37
What is the second stage of inflammation?
Phagocytes are attracted via chemokine and chemotaxis
They destroy any pathogens/ mutated or dead cells
Tissue repair is then happening on damaged cells
38
What are the components of neutrophile granulocytes?
The most common leukocyte in blood
For acute inflamed tissue
Multiple segmented nuclei (granules)
Short lifespan, 5 days
Have antibacterial enzymes e.g lysosomes
39
What are the components of macrophages
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)
40
What are monocytes and where are they found?
Young macrophages, found in the blood
41
Describe the steps in phagocytosis:
Macrophage engulfs microbe by plasma membrane, forming a phagosome (vesicle)
Lysosome attaches and forms a phagolysosome and digests the microbe
Anything indigested is released
42
What are NK cells and what is one way how they work?
Natural killer cells
Kills an infected cell by identifying the cell and killing it
43
What is another way in how an NK cell can kill an infected cell?
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
44
What two receptors do NK cells have?
Activating and Inhibitory receptor
45
Why is there no MHC class 1 when viruses are present?
MHC class 1 is a protein and viruses stop protein production
46
Where does each receptor of an NK cell bind to in a normal cell?
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
47
How does the inhibitory cell binding in an NK cell to a normal cell stop the killing of it?
Binding produces phosphotase which removes phosphate from tyrosine kinases which normally causes the killing
48
How to NK cells kill viruses?
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
49
What does MHC stand for and give another name for it:
Major Histocompatability Complex
Also be called HLA
50
Where is MHC class 1 protein found?
On all cells, marker for all cells
51
Where is MHC class 2 protein found?
On macrophages, B- cells
52
What is the function of MHC 1?
Helps activate only CD8 positive T-cells find antigens and present them on T- cells
53
What is the function of MHC 2?
Helps activate only CD4 positive T-cells, find antigens and present them on T-cells
54
Where are T-cells able to bind?
ONLY things presented in MHC complexes
55
What do B-lymphocytes do?
Block infections and eliminate extracellular microbes
56
What do T-helper lymphocytes do?
Activate macrophages to kill phagocytosed microbes
57
What do T-cytolytic lymphocytes do?
Kills infected cells and illuminate reservoirs of infection
58
Describe one way an antigen is captured and presented by a T-cell:
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
59
Describe another way an antigen is captured and presented by a T-cell:
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
60
What are the functions of immature dendritic cells and where are they found?
Found in the epidermis
They are good at hoovering antigens by makropinocytosis or phagocytosis
61
What are the functions of mature dendritic cells and where are they found?
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
62
How does a Class 2 MHC allow the pathway of intracellular processing of a pathogen?
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
63
How does a Class 1 MHC allow the pathway of intracellular processing of a pathogen?
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
64
What are the differences between an MHC class 1 pathway of intracellular processing and MHC class 2?
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
65
Where are T-cells produced?
Bone marrow
66
Where do T-cells mature and then where do they go after?
Mature in the Thymus and then into secondary lymphatic organs, blood, spleen
67
How are T-cells developed?
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+
68
How are T-cells chosen in positive and negative selection?
If weak (good) bond with MHC II, then CD4+, if weak (good) bond with MHC I, then CD8+, positive selection
69
Why is a weak bond with T-cells and MHC better than a strong bond?
A strong bond leads to activation without antigen and leads to damage, negative selection
70
What type of T-cells are CD4+?
Helper cells
71
What type of T-cells are CD8+?
Cytotoxic cells
72
How is a T-cell replicated from an antigen-presenting cell (APC)?
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
Can a naive T-cell become activated by just binding to the APC and why?
No, needs a co-signal of CD28 – CD80/CD86 which helps with signal transduction
74
What two proteins are needed for adhesion and stabilisation of a T-cell stimulation?
LFA-1 and ICAM1
75
What are the proteins that help with signal transduction of T- cell stimulation?
CD28- CD80/86
CD3 and ITAM
76
What is required for a T-cell interaction can activate?
At least 3 t-cell receptor interactions
77
What are the two T-helper cells called?
Th1 and Th2
78
What is the Th1 cytokine useful for?
Fighting intracellular pathogens
79
What are the two products of Th1 cells?
Interferon gamma
Tumour- Necrosis- Factor (TNF)
80
What is the purpose of interferon gamma?
Th1 marker cytokine
Macrophages: activation and MHC up regulation
Elimination of intracellular bacteria
Antiviral function
81
What is the purpose of TNF?
Macrophages: activation, NO production
Elimination of intracellular bacteria
Dendritic cells: maturation, migration
82
What causes T- helper cells to differentiate into Th1 and Th2?
Th1= IL-12
Th2= IL-4
83
What is the main purpose of Th1 cells?
Activate macrophages
84
What is the induction phase of Th1 helper T-cells?
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
What is the effector phase of Th1 helper T-cells?
INF- gamma leads to activation and increased MHC
TNF- NO production
Lymphotoxin- lysis of infected cells
IL-3/ GM- CSF- production/ differentiation
86
What is the main purpose of Th2 cells?
Activate B-cells
87
What are Th2 T-helper cells useful for?
Important for antibody answer and allergic reactions
88
What are the three products of Th2 cells?
IL-4
IL-5
IL-10
89
What is the purpose of IL-4?
Th2 marker cytokine
Activation/ growth of B-cells
Essential for IgE, Th2 development
Positive feedback, more IL-4, more Th2
90
What is the purpose of IL-5?
B – cell differentiation, IgA synthesis
Growth/differentiation of eosinophils
91
What is the purpose of IL-10?
Regulatory cytokine
Inhibitor of macrophage function, as when Th2, want to rely on antibodies and not macrophages
92
How are naive cytotoxic T-cells activated?
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
Describe the non-secretory mechanism of how a cytotoxic T-cell works:
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
What is a Fas receptor?
A death receptor
95
Describe the secretory mechanism of how a cytotoxic T cell works:
Cytotoxic T cell can release perforin granzyme which makes holes in target cell and kills it
Binding of TCR and MHC still occurs
96
Why is the secretory mechanism unfavoured?
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
What part of the antibody has the antigen binding site?
The variable heavy chain and variable light chain
98
Why is the conserved heavy chain of an Ab important?
This heavy chain is different for different classes of antibodies
99
How many classes of antibodies are there?
Five
100
How do antibodies neutralise a microbe?
They can bind to the microbes and blocks from infecting the cell so prevent microbe from binding to the receptor
101
Name the five types of antibodies:
IgA, IgG, IgE, IgD, IgM
102
What is the anti body involved in first primary response?
IgM
103
What is the antibody involved in the secondary response?
IgG
104
What are the different fragments in the variable region?
V, D, J,
105
What is junctional diversity?
Adding or subtracting nucleotides as this changes the protein sequence which creates more diversity in antibodies
106
What is the name given for production of the variable region on the heavy chain and how is this done?
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
What is the production for the variable region of the light chain?
The same as for the heavy chain but the D segment isn't involved
108
What is somatic hyper mutation and name three ways this is done:
Different ways antibody changed once displayed:
1. Affinity maturation
2. Switch from membrane to secreted form
3. Isotype switching
109
What is affinity maturation?
Small mutation over time inside the antibody which should increase the affinity and make a better antibody
110
What is switching from membrane to secreted form?
The antibody is released to the blood stream so it can find antigens and bind to them
111
What is isotope switching?
Replace constant region of the antibody (heavy chain) so changes class of Ab
112
Where are B cells made and how do they mature?
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
How do B cells undergo isotope switching?
Have switch regions which recombination can occur by looping out
114
Describe the primary antibody response:
Naive B cell- activated
Ab secreting cells release IgM, some IgG formed
After, low levels of IgG and plasma cells around
115
Describe the repeat infection response of an antibody:
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
What are three characteristics of memory B cells?
Only secretion of IgA, IgG and IgE
Enhanced Ab affinity compared to naive
Increased somatic hypermutation
117
What are three characteristics of memory T cells?
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
What is an allergy?
And unwanted inflammatory and immune response
119
Name and describe predisposing factors which favours atopic phenotypes:
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
State and describe the types of hypersensitivity reactions:
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
What is an important mast cell growth factor? Type 1
Stem cell factor (SCF)
122
Where are mast cells differentiated and found? Type 1
Differentiation in tissue
Found in connective tissue
123
What receptors do mast cells contain for IgE? Type 1
FcERI
124
Why are mast cells important in the innate immune system? Type 1
– 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
Whats the initiation of a type 1 immune response?
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
How does IgE trigger a type 1 allergic reaction?
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
What is degranulation?
Granules in mast cells, containing histamines, are released which leads to an immediate hypersensitivity reaction
128
What happens when mast cells are activated in the GI tract?
An increase in fluid secretion therefore expulsion of GI contents E.G. diarrhoea/vomiting
129
What is a late phase reaction in type one hypersensitivity?
4 to 16 hours after being exposed to the allergen a less significant reaction occurs
130
Describe anaphylactic shock: Type1
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
What is the treatment for anaphylactic shock? Type 1
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
What are the complications of an anaphylactic shock? Type 1
Heart arrhythmias, shock, cardiac arrest, airway obstruction
133
Give an example of type II hypersensitivity and what occurs during it?
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
Give an example of type III hypersensitivity and what occurs during it?
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
Give an example of type IV hypersensitivity and when does it occur?
E.G. contact dermatitis
Occurs 24-48 hours after, also called delayed-type hypersensitivity
136
What is the difference between type IV hypersensitivity and all the other hypersensitivities?
It's a T-cell mediated and not antibody-mediated
137
What occurs during type IV hypersensitivity?
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
What test can be used to determine a Type IV hypersensitivity and give an example:
Mantoux test- test whether allergic or not
Tuberculin skin test- injecting a small amount of substance into forearm
139
Which histamine receptor is found on the smooth muscles and what is the effect of histamine on them?
H1, from the constriction, contraction of GI tract
140
Which histamine receptor is found on the endothelium and what is the effect of histamine on them?
H1, vasodilation, increasing capillary permeability which leads to oedema
141
Which histamine receptor is found on the sensory nerve endings and what is the effect of histamine on them?
H1, pain and itching
142
Which histamine receptor is found on smooth muscles of the blood vessel and what is the effect of histamine?
H2, vasodilation
143
Which histamine receptor is found on immune active cells and what is the effect of histamine?
H4, chemotaxis
144
What are three things that can reduce the effects of released histamines?
1. Physiological antagonists
2. Histamine release inhibitors
3. Histamine receptor antagonists/antihistamines
145
How do physiological antagonist work against histamines?
e.g. epinephrine
Smooth-muscle actions opposing histamine but acts on different types of receptors, not histamine receptors
146
Name two histamine release inhibitors:
a) Mast cell stabilisers
b) Beta 2 adrenergic agonists
147
What are first-generation antihistamines and how do they work?
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
What are second generation antihistamines and how do they work?
Nonsedating, poorly penetrate the blood brain barrier
Rapidly absorbed by the GI tract, widely distributed
Elimination – cetrizine, urine
– Fexofenadine, bile
149
Which type of antihistamines have an anticholinergic affect and what does this mean?
First generation, inhibit responses to Ach that are mediated by muscarinic receptors
Effects are dry mouth, blurred vision, constipation
150
Which type of antihistamine has an effect on the CNS and how does it do this?
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
Give three drug interactions with with first-generation H1 antihistamines:
– 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
Give three examples of second-generation histamine receptor antagonists:
Fexofenadine, loratadine, cetirizine
153
Give two examples of mast cell stabilisers and how are they used?
Cromolyn and Nedocromyl
Not orally absorbed, so given as a powder by inhalation
Inhibit histamine release by inhibiting chloride channels on mast cells
154
What are mast cell stabilisers used for and give side-effects:
Against bronchial asthma and allergic rhinitis
SE = dry mouth, throat irritation, cough/wheeze
155
Which immune system is the complement system in even though it has antibodies involved?
Innate
156
What is the difference in specificity between the innate and adaptive IS?
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
What is the difference in receptors between the innate and adaptive IS?
Very few receptors in innate e.g mannose, toll like and N-formyl methionyl
In adaptive there is somatic recombination so greater diversity
158
Describe the structure of T cell receptors:
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
Which cells express MHC class 1?
On all cells with a nucleus
High expression on lymphocytes
Low expression on non lymphoid cells
160
Which cells express MHC class 2?
Not on all cells
High expression on antigen presenting cells e.g dendritic, macrophages and B cells
Activated T cells
161
Where does MHC class bind to?
Only stable on cell surface with peptide
162
Where are immature dendritic cells found?
Epidermis
163
Where are mature dendritic cells found?
T cell rich areas like lymph nodes and spleen
164
Why is somatic recombination called that?
Somatic as happens in B cells
165
State 4 ways in which antibody diversity is reached:
Combination of gene segments
Junctional diversity
Combination of different heavy/ light chains
Somatic hypermutation
166
Describe the difference in reactions when exposed to an antigen in the different ISs:
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
What is an allergen?
A substance that is recognised by the immune system and cause an allergic reaction
168
What is an allergen?
A substance that is recognised by the immune system and cause an allergic reaction
169
State what happens in a type 1 hypersensitivity reaction and what are the symptoms because of it:
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
What characteristics do allergens have that favours a Th2 response?
Proteins
Active enzymes- proteases
Low dosage
Low molecular weight as can diffuse into mucosa
Good solubility
171
Name and describe products which can be released by activated mast cells:
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
What is atopy?
The genetic predisposition to make IgE antibodies in response to allergen exposure patients prone to IgE mediated allergic reactions are said to be atopic
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State people more prone to allergen exposure:
Males
Small familes
Prenatal diet and smoking
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What is the atopy phenotype:
Genes on chromosomes 5 and 11
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Describe the lymph system:
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
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What does the spleen do?
Collects antigens from the blood stream
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How does ibuprofen and aspirin work?
Inhibits COX 1 and 2
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What type of receptors do macrophages have on them and how many different kinds are there?
Toll like receptors
At least 10
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What other receptors do macrophages have and how do they work?
Have GPCR's which bind to other chemokine which cause macrophages to migrate into tissue, to site where bacterial infection is
