15. Immune System Flashcards
Unedited (230 cards)
1
Q
What is the immune system?
A
A versatile defence system that protects us from pathogenic microbes
2
Q
What are the layers of the defence strategy?
A
- First line - innate immunity (barrier)
- Second line - innate immunity (response)
- Third line - specific/adaptive immunity
3
Q
What is the first line of defence - innate immunity?
A
Physical barrier created by the skin and mucous membranes*
and associated secreted chemicals
4
Q
What is the second line of defence - innate immunity?
A
Non-specific immune response that includes some immune cells, proteins, fever and inflammation
5
Q
What is the third line of defence - specific/adaptive immunity?
A
Activated by the innate immune system, producing a response towards a specific pathogen
6
Q
What is a pathogen?
A
An infectious agent that can cause disease in a host
Microbes
Macro-organisms (e.g parasitic worms)
7
Q
How can pathogens enter the body?
A
Breaks in the skin Respiratory system Digestive system Reproductive system (male and female) Eyes
8
Q
What is an antigen*?
ANTIbody GENerator
A
A substance that can be recognised by leukocytes
Antigens can stimulate an immune response to defend the body
9
Q
What are the two types of antigen?
A
- Foreign antigens
- Self-antigens*
The immune system is usually tolerant of self-antigens,
10
Q
What are foreign antigens?
A
Microbes
Food
Drugs
11
Q
What are self-antigens?
A
Found on cell membranes
Transmembrane protein, produced by the cell*
*via DNA transcription, translation
12
Q
What do antigens usually consist of?
A
Proteins (specific 3D shape)
13
Q
What are antibodies?
A
Proteins produced in response to a specific antigen
14
Q
What do antibodies and the specific antigens do?
A
Combine, creating an ‘immune response’
15
Q
What makes the skin a first line of defence against pathogens?
A
Made up of layers of tightly packed epithelial cells
Outer epidermis - consists of dead epithelial cells are constantly being shed to remove microbes
Dermis - contains accessory structures such as sebaceous glands and sweat glands
16
Q
How does sweat perform an immune function?
A
Removes microbes from skin
Contains IgA antibodies*
Immunoglobulin A : also in salivia, tears and breastmilk
17
Q
How does sebum perform an immune function?
A
Contains fatty acids which inhibit microbial growth
*stop mitosis in bacteria
18
Q
Where can mucous membranes be found?
A
- Digestive tract
- Respiratory tract
- Urogenital tract
- Conjunctiva
19
Q
What is the function of mucous membranes?
A
Prevent entry of pathogens into the membrane
20
Q
How do the mucous membranes perform an immune function?
A
Mucous traps microbes and foreign particles
Saliva, tears and mucous secretions wash away the trapped microbes
They also contain anti-microbial substances
21
Q
How does the immune function work in the respiratory tract?
A
Mucocillary escalator
Cilia propel any foreign substances towards the pharynx where they are swallowed or coughed up
22
Q
How do tears and saliva perform an immune function?
A
Contain IgA and lysozymes
Lysozymes are enzymes that break down bacterial cell walls
23
Q
How does the nose perform an immune function?
A
Hairs in the nose filter air
24
Q
How does the vagina perform an immune function?
A
In menstruating women, vagina is acidic making it unfavourable for microbes
25
How does gastric acid perform an immune function?
Acidity destroys many bacteria
| pH 2-3
26
How do microflora perform an immune function?
Outcompete pathogens for
* attachment sites on epithelial cell surfaces (esp in large intestine*)
* essential nutrients
| *Proximity to GALT aids learning for lymphocytes
27
How does the excretion of urine and faeces perform an immune function?
Both expel microbes
28
How does vomiting and diarrhoea perform an immune function?
Both rapid means of expelling pathogens
29
When does the second line of defence get activated?
When pathogens penetrate the physical and chemical barriers of the skin and mucous membranes
30
What does the second line of defence consist of?
```
Transferrins
Complement system
Phagocytes
Natural killer cells
Inflammation
Cytokines
Fever
```
31
What are transferrins?
Iron-binding proteins in blood*
| In haemoglobin
32
How do transferrins work?
Inhibit the growth of certain bacteria by reducing the amount of available iron
33
Why are transferrins necessary?
Without transferrins, bacteria would use the iron available for their growth
| Bacteria love iron. Supplements should be avoided during infection
34
What is the complement system?
Secondary defence system
Over 30 proteins*
Circulating in the blood in their inactive (full) form
| * produced by the liver
35
How are complement proteins identified?
By a letter (mostly C) and a number e.g. C3
36
How does a complement protein start out?
Inactive
Become active when split by enzymes into active fragments
e.g. C3 >>> C3a and C3b
37
What happens when a complement protein is activated
Acts in a cascade
38
What is the most common mechanism through which complement proteins are activated?
Classical pathway
39
What is the 'classical pathway'?
Antigens and antibodies join together
>Forming an antigen-antibody complex
>>This triggers the immune response (cascade)
40
What is the role of complement proteins?
1. Promoting phagocytosis
2. Contributing to inflammation
3. Causing cytolysis
41
How do complement proteins promote phagocytosis?
The fragment C3b coats a microbe in a process called opsonisation
This promotes the attachment of a phagocyte to a microbe
42
How do complement proteins contribute to inflammation?
C3a and C5a bind to mast cells and cause them to release histamine
43
How do complement proteins cause cytolysis?
The final 5 complement proteins join together and create a hole in the foreign cell
The hole fills with tissue fluid and makes the cell swell and rupture
44
What are cytokines?
Small protein hormones that stimulate or inhibit normal cell functions
Mediate the connection between the innate immune system and the adaptive immune system
45
What are cytokines secreted by?
Leukocytes
46
What are the types of cytokines?
Interleukins
Interferons
Tumour necrosis factor
47
# cytokines
What are interleukins?
Mostly produced by T-helper cells
Mediators between leukocytes
| e.g IL-1 released by macrophages > hypothal > inc in temp
48
# cytokines
What are interferons?
Anti-viral proteins produced by cells that are infected by a virus
| Tell surrounding cells to stop dividing (viruses do not self-replicate)
49
# cytokines
What does tumour necrosis factor do?
Promotes the accumulation of neutrophils and macrophages to an area
Causes cell death
50
# cytokines
How do interferons work?
They diffuse to uninfected neighbouring cells and induce synthesis of anti-viral proteins that interfere with viral replication
51
# cytokines
Do interferons stop a virus attaching to it?
No but they prevent the virus from replicating
52
What do phagocytes do?
They perform phagocytosis - cell digestion - of anything they don't recognise*
Non-selective
| *Any cell with a foreign antigen
53
How do phagocytes work?
By engulfing and digesting cells
Using their lysozymes to break down the pathogen
It then displays a piece of the pathogen on its membrane
54
What is chemotaxis?
Directed migration* of a cell in response to a chemical stimulus
| *to a site of inflammation
55
What are the two major types of phagocyte?
Neutrophils
Macrophages
56
What do neutrophils do?
First to migrate to a scene of inflammation
Like neighbourhood watch
Try to mop up the day to day problems
57
What do macrophages do?
They follow the neutrophils and eat up the remnants of whatever needs to be broken down and digested
They engulf and digest the pathogen, excrete some of the waste and display the rest on the cell membrane to present to T-lymphocytes
58
Where can macrophages be found?
In tissue
59
Where can monocytes be found?
In blood
60
What do monocytes do?
Migrate to the site of infection and enlarge to form wandering macrophages
61
What do fixed macrophages do?
Stand guard in specific tissues
62
In which tissues can fixed macrophages be found?
Histiocytes (connective tissue macrophages)
Kupffer cells - liver
Microglia - nervous tissue
Alveolar - lungs
Langerhans cells - skin
Tissue macrophages - spleen, bone marrow, lymph nodes
63
What are the stages of phagocytosis?
1. Chemotaxis - release of chemicals by leukocytes, damaged tissue and activated complement that attract phagocytes
2. Adherence - attachment of phagocyte to target (aided by complement)*
3. Ingestion - cell membrane extends to engulf the microbe
4. Digestion - ingested structure merges with lysozymes to be digested
5. Excretion - ingested material is excreted
| *Some bacteria (eg TB) resistant to adherence - therefore phagocytosis
64
What are natural killer cells?
Non-specific lymphocytes
65
What percentage of lymphocytes do natural killer cells make up?
5-10%
66
Where can natural killer cells be found?
Blood
Lymph nodes
Spleen
Bone marrow
67
How do natural killer cells work?
They attack anything that they don't recognise including abnormal body cells e.g. cancerous cells*
They bind to a target cell and release granules containing the protein perforin
| Cancerous cells display abnormal surface antigens on their membranes
68
What does perforin do?
It inserts into the cell membrane and creates a channel for tissue fluid to flow into the cell - cytolysis
69
What is inflammation?
A non-specific defensive response to tissue damage
70
What can inflammation be caused by?
* Pathogens (infection)
* Abrasions
* Chemicals
* Cell distortion/disturbance
* Extreme temperatures
| Importantly, the response to different insults is the **same**
71
What response does inflammation create?
Non-specific, systemic response
Acts as an alarm attracting immune cells to the area
72
What are the 5 cardinal signs of inflammation?
```
Redness
Heat
Pain
Swelling
Loss of function
```
73
# Second line of defence: Non-specific immune reactions
What are the stages of inflammation?
1. Vasodilation and increased permeability
2. Migration of phagocytes
3. Tissue repair
74
# Second line of defence: Non-specific immune reactions
How does vasodilation help inflammation?
Allows additional blood, oxygen, nutrients, immune cells and repair substances to get to the area quicker
Quicker removal of toxins and dead cells
75
# Second line of defence: Non-specific immune reactions
How does increased permeability help inflammation?
Permits the movement of immune cells, defensive proteins (antibodies) and clotting factors into the tissue
76
# Second line of defence: Non-specific immune reactions
What is created by vasodilation and increased permeability ?
Redness, swelling and heat
77
# Second line of defence: Non-specific immune reactions
What is the pain of inflammation a result of?
Injury to neurons and toxic chemicals released by microbes
78
# Second line of defence: Non-specific immune reactions
What happens when phagocytes migrate to an area?
1. Phagocytes migrate to the scene (via chemotaxis)
2. Neutrophils stick to the endothelium during vasodilation and squeeze through the vessel wall to reach the damaged area
3. Monocytes quickly follow and transform into wandering macrophages
4. Dead phagocytes accumulate pus
79
# Second line of defence: Non-specific immune reactions
What are the types of inflammatory mediators?
Histamine
Leukotrienes
Kinins
Prostaglandins
80
# Second line of defence: Non-specific immune reactions
What is histamine and its function?
Released by mast cells and basophils
Causes vasodilation and increased permeability
81
# Second line of defence: Non-specific immune reactions
What are leukotrienes and their function?
Released by basophils and mast cells
They attract phagocytes and increase permeability
82
# Second line of defence: Non-specific immune reactions
What are kinins and their function?
Proteins
Causes vasodilation and increased permeability
Also attract phagocytes and induce pain
83
# Second line of defence: Non-specific immune reactions
What are prostaglandins and their function?
Lipids released by damaged cells
Enhance effects of histamine and kinins (intensifying the pain)
84
# Second line of defence: Non-specific immune reactions
What are the benefits of inflammation?
Promotes phagocytosis through increased temperature
Promotes immune response via vasodilation/permeability
Dilutes toxins
Fibrin formation - isolates affected area and helps bind wound edges
85
# Second line of defence: Non-specific immune reactions
What are the harmful effects of inflammation?
Swelling - dangerous if in cranium
Pain - can become chronic
Adhesions and scar tissue
Atherosclerosis
86
# Second line of defence: Non-specific immune reactions
What are the outcomes of inflammation?
Resolution
Chronic inflammation
Granuloma
Fibrosis
87
# Second line of defence: Non-specific immune reactions
What is chronic inflammation?
If the injury-causing agent persists
Can cause chronic pain
Prevalence of macrophages, plasma cells and lymphocytes
88
# Second line of defence: Non-specific immune reactions
What is granuloma?
Cellular attempt to contain a foreign body through aggregation of macrophages surrounded by lymphocytes
| eg TB is resistant to phagocytosis
89
# Second line of defence: Non-specific immune reactions
What is fibrosis?
Replacement of functional tissue with non-functional scar tissue
Formed by the secretion of collagen by fibroblasts
Occurs as a result of chronic inflammation
90
# Second line of defence: Non-specific immune reactions
What is a fever?
An abnormally high body temperature, creating unfavourable environment for pathogens
91
# Second line of defence: Non-specific immune reactions
How does a fever occur?
Because the hypothalamus thermostat is reset to a higher temperature
Allowing body core temperature to rise
92
# Second line of defence: Non-specific immune reactions
When is a fever most likely to occur?
In infection and inflammation
93
# Second line of defence: Non-specific immune reactions
What happens pathophysiologically during a fever?
Bacterial toxins elevate body temperature which triggers release of fever-causing cytokines
e.g. interleukin-1from macrophages
94
# Second line of defence: Non-specific immune reactions
What is the key function of interleukin-1?
To induce fever
By signalling to the hypothalamus to raise body temperature
95
# Second line of defence: Non-specific immune reactions
What does an elevated body temperature do?
* Makes interferons more effective
* Inhibits growth of some microbes
* Speeds up the reactions that aid repair
96
# Second line of defence: Non-specific immune reactions
What can be granular or agranular?
Leukocytes
97
# Second line of defence: Non-specific immune reactions
Which leukocytes are classed as granular?
Basophils (mast cells)
Eosinophils
Neutrophils
98
# Second line of defence: Non-specific immune reactions
Where can you find basophils?
In blood
99
# Second line of defence: Non-specific immune reactions
Where can you find mast cells?
In tissue
100
# Second line of defence: Non-specific immune reactions
What do basophils and mast cells do?
Release histamine and heparin
Release leukotrienes
Express receptors for IgE*
| Involved in allergy/hypersensitivity
101
# Second line of defence: Non-specific immune reactions
What does histamine do?
Causes vasodilation
Increases vessel permeability
102
# Second line of defence: Non-specific immune reactions
What does heparin do?
Anti-coagulant
Involved in inflammations
103
# Second line of defence: Non-specific immune reactions
What do eosinophils do?
Destroy parasitic worms via phagocytosis
Play a role in inflammation (central in asthma)
104
# Second line of defence: Non-specific immune reactions
What do neutrophils do?
Phagocytic cell
Granules release lysozymes that digest debris
105
# Second line of defence: Non-specific immune reactions
Which is the most abundant leukocyte?
Neutrophils (60%)
106
Which leukocytes are classed as agranular?
Monocytes/macrophages
Natural killer cells
B and T lymphocytes
107
# Second line of defence: Non-specific immune reactions
Where can you find monocytes?
In blood
108
# Second line of defence: Non-specific immune reactions
Where can you find macrophages?
In tissue
Can be wandering or fixed
109
# Second line of defence: Non-specific immune reactions
What do monocytes/macrophages do?
Phagocytic
Secrete cytokines e.g. IL-1 and TNF
110
# Second line of defence: Non-specific immune reactions
What do natural killer cells do?
Target foreign cells
Secrete perforin to induce cytolysis
111
# Third line of defense: Specific immunity
What are B and T lymphocytes?
| Lymphocytes live in the lymph (formed in the red blood marrow)
Effector cells of the adaptive (specific) immunity
112
# Second line of defence: Non-specific immune reactions
Which leukocytes are phagocytic?
Neutrophils
Monocytes/macrophages
113
# Third line of defense: Specific immunity
Name the different types of T-lymphocytes*
| T-lymphocytes mature in the Thymus
Cytotoxic T-cells (CD8)
Helper T-cells (CD4)
Memory T-cells (only created after active exposure)
Regulatory T-cells (to stop excessive reactions)
114
# Third line of defense: Specific immunity
What do helper T-cells do?
Mediates the immune response
115
# Third line of defense: Specific immunity
What do cytotoxic T-cells do?
Immune cells out in the field
116
# Third line of defense: Specific immunity
What do memory T-cells do?
Create a memory of a pathogen after they've been exposed to it
117
# Third line of defense: Specific immunity
What do regulatory T-cells do?
Turn off the immune response when it's finished to avoid excessive reactions
118
# Third line of defense: Specific immunity
Where are T-cells produced/mature?
Produced in bone marrow
Mature in the thymus
119
# Third line of defense: Specific immunity
Name the different types of B-lymphocytes
Plasma cells
Memory B-cells
120
# Third line of defense: Specific immunity
Where are B-cells produced/mature?
In red bone marrow
121
# Third line of defense: Specific immunity
Where do T-cells and B-cells function?
In the 3rd line of defence
Adaptive (specific) immunity
122
# Third line of defense: Specific immunity
How do T-cells and B-cells know how to respond to foreign antigens?
Through learning
They usually can tell the difference between self and non-self antigens
123
# Third line of defense: Specific immunity
Which sort of pathogens do T-cells and B-cells go after?
Specific ones
124
# Third line of defense: Specific immunity
How do T-cells and B-cells know which antigens they've met before?
Through immune memory
125
# Third line of defense: Specific immunity
What does immune memory allow T-cells and B-cells to do?
Produce a quicker and more effective attack next time they encounter the pathogen
126
# Third line of defense: Specific immunity
When is the 3rd line of defence activated?
When the 1st and 2nd lines fail to destroy the pathogen
| Otherwise they are resting
127
# Major Histocompatibility Complexes
What are major histocompatibility complexes (MHC)?
Group of proteins on cell surface that are used by the immune system to recognise cells that are self cells vs non-self
128
# Major Histocompatibility Complexes
What are MHCs formed from?
4 polypeptide chains
129
# Major Histocompatibility Complexes
How do MHCs work?
They display a protein (a self-antigen) produced by the cell on its binding groove
130
# Major Histocompatibility Complexes
How do MHCs help T-cells?
By presenting foreign antigens to T-cells
131
# Major Histocompatibility Complexes
Name the two types of MHC
1. Class I Major Histocompatibility Complex (MHC-I)
2. Class II Major Histocompatibility Complex (MHC-II)
132
# Major Histocompatibility Complexes
Where can you find MHC-I?
On all body cells except erythrocytes
133
# Major Histocompatibility Complexes
How do MHC-I work?
Essentially our self-antigen.
When body cell is cancerous or invaded by pathogen, the cell starts to produce abnormal proteins
These proteins are combined with MHC-I and displayed on the cell membrane
Flags up to (mostly) cytotoxic T-cells (CD8) as a non-self antigen
134
# Major Histocompatibility Complexes
Where can you find MHC-II?
Only on the cell membrane of 'antigen presenting cells':
* macrophages
* B-lymphocyte
135
# Major Histocompatibility Complexes
How do MHC-II work?
The MHC-II displays the foreign antigen on its binding groove, having ingested the foreign cell
136
# Major Histocompatibility Complexes
What are MHC-II specifically used for?
Communication between themselves and T-helper cells
They present the antigen to the T-helper cells as part of antigen presentation
137
# Major Histocompatibility Complexes
How does an antigen become associated with MHC-I or II
By the route it's trafficked through the cell
138
Which type of immunity do T-cells play a central part in?
Cell-mediated immunity
139
What is unique about T-cells?
Each has a unique T-cell receptor (TCR) that only recognises a specific antigen
140
What are T-helper cells also known as?
CD4 cells
| because they express the CD4 protein on their surface
141
What are cytotoxic T-cells also known as?
CD8 cells
142
To function properly, which traits should T-cells have?
Self-recognition - to recognise self antigens
Self-tolerance - must lack reactivity to fragments of self antigens
143
What does a lack of self-tolerance lead to?
Autoimmunity
144
How are T-cells tested?
Against epithelial cells in thymus
Should be able to recognise self antigens
145
What happens to T-cells if they don't recognise self antigens?
They undergo apoptosis
146
What percentage of T-cells make it through the maturing process?
1-5%
147
What is adaptive immunity?
Ability of the body to defend itself against specific foreign cells
148
What is adaptive immunity characterised by?
Specificity for particular foreign antigens
Production of immune memory
| ```
```
149
What are the two types of adaptive immunity?
1. Cell-mediated
2. Antibody-mediated
150
What is cell-mediated immunity?
Driven by T-cells
Cytotoxic T-cells directly attack specific invading antigens
Mostly against intracellular pathogens
151
What is antibody-mediated immunity?
Driven by B-cells
B-cells transform into plasma cells, which synthesise and secrete specific antibodies (Igs)
Mostly against extracellular pathogens
152
What happens during antigen presentation?
1. Antigen presenting cells break down the antigen into fragments (using lysozymes)
2. Some fragments are combined with MHC-II molecules on their cell membrane
3. They migrate into lymphatic tissue where they present the antigen to T-helper cells
4. Antigen fragment binds with the T-helper cell
5. T-helper cell secretes a cytokine called interleukin-2 (IL-2)
6. Interleukin-2 causes the T-helper cell to undergo clonal selection
153
What happens during clonal selection of T-cells?
Division and proliferation of activated T-cells
154
What does the process of T-cell clonal selection produce?
1. Cytotoxic T-cells that bind to target cell and destroy it using **granzymes** and **perforin**
2. Memory T-cells - these are inactive but will recognise the antigen in the future if it appears again
3. Helper T-cells that release cytokines which increase the activity of immune cells such as T, B and NK cells
155
What do granzymes do during T-cell clonal selection?
Break down the foreign cell
156
What does perforin do during T-cell clonal selection?
Burst the foreign cell
157
Why are regulatory T-cells important?
Without them the body would continue to fight off a disease that no longer exists and could end up fighting its own cells
Maintain **immunity homeostasis**
Implicated in autoimmune diseases
158
# Antibody mediated immunity
What happens during antibody mediated immunity?
1. Antigen binds to specific B-cell receptors
2. It's taken into the cell and broken down into fragments
3. Fragments are expressed on the MHC-II
4. Helper T-cells recognise the antigen complex on the B-cell membrane and stimulate it by releasing IL-2 which triggers B-cell clonal selection
159
# Antibody mediated immunity
What types of cell does B-cell clonal selection produce?
Plasma cells - secrete antibodies into blood, short lived
Memory B-cells - remain inactive until next immune reaction, long lived
160
# Antibody mediated immunity
Which group of glycoproteins do antibodies belong to?
Globulins/immunoglobulins
161
# Antibody mediated immunity
How are antibodies structured?
4 polypeptide chains - 2 heavy, 2 light
Variable region for each type of antibody
2 antigen binding sites
162
# Antibody mediated immunity
What do antibodies combine with?
The antigen that triggered their production
163
# Antibody mediated immunity
What does the combining of an antibody with an antigen produce?
Antibody-antigen immune complex
164
# Antibody mediated immunity
How to antibodies inactivate antigens?
1. Neutralising
2. Immobilising
3. Agglutinating and precipitating
4. Activating complement
5. Enhancing phagocytosis
165
# Antibody mediated immunity
What happens when antibodies neutralise an antigen?
Neutralises bacterial toxins or prevent viral attachment to cells
166
# Antibody mediated immunity
What happens when antibodies immobilise an antigen?
Binds to it on bacterial cilia or flagellae
167
# Antibody mediated immunity
What happens when antibodies agglutinate and precipitate an antigen?
Antibodies use both of their binding sites to cause a clumping of cells
168
# Antibody mediated immunity
What happens an antibody activates complement?
Antigen-antibody complexes activate the complement cascade
169
What happens when antibodies enhance phagocytosis?
Antibody acts as a flag to attract phagocytes and aids phagocytosis via agglutination and complement
170
What are the 4 different types of antibodies?
IgG
IgA
IgM
IgE
171
IgG - location, how common, function?
Blood, lymph, intestines
Most abundant (80%) of blood antibodies
Protects against viruses and bacteria
Crosses placental barrier
172
IgA - location, how common, function?
Sweat, tears, saliva, breast milk
10% of blood antibodies
Localised protection of mucous membranes
Decreases with stress
173
IgM - location, how common, function?
Blood, lymph
10% of blood antibodies
Early immune response (first on site)
174
IgE - location, how common, function?
Blood
0.1% blood antibodies
Allergic reactions
Binds to mast cells (to release histamine and heparin)
175
What happens during the primary response of immunological memory?
Slow response
Antibodies start to appear after several days
Slow rise in IgM, followed by IgG
176
What happens during the secondary response of immunological memory?
Faster response as a full immune response has been developed in the memory cells
Usually so quick, the pathogen is killed off before any signs and symptoms present
177
How do vaccinations help the immune system?
By creating immunological memory against the specific disease the vaccination covers
178
What do vaccinations contain?
Weakened, whole or partially-killed portions of microbes
179
What happens after a vaccination is given?
B and T-cells are activated in a primary response
Can take several days
180
In what 4 ways can you acquire immunity?
1. Naturally acquired active immunity
2. Naturally acquired passive immunity
3. Artificially acquired active immunity
4. Artificially acquired passive immunity
| Passive because body is not generating antibodies
181
What is naturally acquired active immunity?
Natural exposure to a disease
182
What is naturally acquired passive immunity?
Transfer of IgG antibodies across the placenta from mother to child
Transfer of IgA antibodies from mother to child via breast milk
| Passive because body is not generating antibodies
183
What is artificially acquired active immunity?
Vaccination
184
What is artificially acquired passive immunity?
Injection with immunoglobulins e.g. snake anti-venom
| Passive because body is not generating antibodies
185
What cells can be found in GALT?
Macrophages
B and T-cells
186
Where can GALT be found?
Tonsils
Oesophagus
Small intestine
Large intestine
187
What is a hypersensitivity reaction?
An excessive immune response produced by the normal immune system
188
What are the 4 types of hypersensitivity?
Type I, II and III - antibody mediated
Type IV - cell mediated*
| T-cells
189
What is Type I hypersensitivity?
An allergy
190
What is a Type I hypersensitivity mediated by?
IgE antibodies that bind to mast cells
Causes
* degranulation
* histamine response
191
What are the 2 types of Type I hypersensitivity reactions?
1. Systemic e.g. anaphylaxis
2. Localised e.g. hay fever, eczema, irritant contact dermatitis
192
How soon is there a Type I hypersensitivity response?
Immediate - within minutes of exposure
193
What is Type II hypersensitivity?
Blood transfusion reactions
Haemolytic disease of the newborn
194
What is a Type II hypersensitivity mediated by?
IgG antibodies which bind to antigen and activate the complement system
195
How soon is there a Type II hypersensitivity response?
Rapid onset
196
What is a Type III hypersensitivity mediated by?
IgG
IgA
IgM antibodies
197
How soon is there a Type III hypersensitivity response?
Within 4-8 hours
198
In which pathologies does a Type III hypersensitivity reaction occur?
RA
Systemic lupus erythematosus (SLE)
Glomerulonephritis
199
What happens in a Type III hypersensitivity reaction?
Antibody-antigen complexes form and deposit in capillaries, skin, kidneys, joints etc triggering an immune response
They activate the complement system
200
What is a Type IV hypersensitivity mediated by?
Cells
201
What happens in a Type IV hypersensitivity reaction?
* Overreaction of T-cells to an antigen
* Large numbers of cytotoxic T-cells activated
* Cytokines released that can damage normal tissue
202
How soon is there a Type IV hypersensitivity response?
48-72 hours
203
What is an allergy?
A powerful immune response to an allergen
204
What is an allergen?
An antigen that generates allergy
Usually harmless
205
How does an immune response towards an allergy develop?
1. Initial exposure causes sensitisation
Slow response as not many cells have learnt how to respond yet to that antigen
2. Subsequent exposure is a quicker and much, more exaggerated response
The full immune response has been developed and antibodies are readily available.
206
How does the body prepare for an allergen response?
Body produces IgE specially for that antigen:
1. B-cell plasma cells activated
2. Antibodies produced targeting that specific antigen
3. Y-shape: one side binds to the antigen, the other side to the mast cell
207
What are the symptoms of an allergy?
Mild to fatal!
Runny nose
Streaming eyes
Anaphylaxis
208
What percentage of adults are affected by a food allergy?
2%
209
What percentage of children are affected by a food allergy?
6%
210
What is a food allergy?
An IgE-mediated immune response
| IgE will be present in response to ingestion of food allergen
211
How is food intolerance different to an allergy?
Food intolerance doesn't have a defined immune response
| However, poor digestion can *lead* to allergic (IgG mediated) reactions
212
What is a food intolerance?
Symptoms triggered by eating a quantity of food and lacking the enzymes/probiotics/bile/HCI and other digestive factors needed to deal with the food
213
What is missing if a person is lactose intolerant?
The enzyme lactase
214
What is anaphylactic shock?
Severe, systemic, allergic response to an allergen exposure
215
How soon can anaphylactic shock appear?
Within 5-10 mins
216
What happens in the body to create anaphylactic shock?
1. Exposure to allergen causes IgE to activate mast cells and basophils
2. Systemic granulation of mast cells histamine is released
3. Causes bronchoconstriction, vasodilation and oedema of tissue
217
Why is anaphylactic shock dangerous?
Can cause occlusion of the airways
218
What is the treatment for anaphylactic shock?
EpiPen (Epinephrine)
219
What is the difference between acute and chronic inflammation ?
Acute inflammation is physiological (and beneficial)
Chronic inflammation is pathological
220
Which cells produce antibodies ?
Plasma cells
(B-lymphocytes)
221
Qualites of plasma cells
* Secrete antibodies into the blood
* Only produce one type of antibody
* Secrete hundres of millions of antibodies each day (until cell dies)
* Short-lived
222
Qualities of Memory B-cells
Long-lived
Remembers the antigen for next time
Ready to proliferate and produce more plasma cells for a second immune reaction
223
How long can memory cells last ?
Decades
224
What separates GALT from microflora in the gut ?
Single epithilial cells
GALT is in the lamina propria
Provides learning environment for B and T cells
225
Where can Type IV hypersenstive reactions be observed ?
Skin graft rejections
Allergen contact dermatitis
Multiple Sclerosis (MS)
226
What causes vasodilation and increased permeability during inflammation ?
| Not on slides
Histamine and heparin released by degranulated mast cells
227
Which cell do macrophages and B-lymphocytes display antigens to ?
T-lymphocytes
228
Which cells are antigen-presenting ?
Macrophages
B-lymphocytes
229
What is antigen presentation ?
Where macrophages display a piece of a digested pathogen on its cell membrane
T-lymphocytes are then able to receive and learn about what foreign antigens are present in the body
230
What is opsonisation ?
The process of coating a microbe with C3b in order to attach phagocytes
