Immunology and Immunopathology Flashcards
(99 cards)
1
Q
Label the diagram.
A
- Pluripotent Stem Cell
- Common lymphoid progenitor
- Myeloid progenitor
- Megakaryocyte
- Platelets
- T-cell Precursor
- B-cell Precursor
- Natural Killer Cell
- B-cell
- Erythroblast
- Erythrocyte
- Neutrophil
- Basophil
- Eosinophil
- Monocyte
- Thymus
- T cell
- Macrophage
- Dendritic Cell
- Mast Cell
- Bone Marrow
- Periphery
- Blood
- T-dependant area of the lymph nodes and spleen
- B-cell areas of the lymph nodes, spleen, Peyer’s patches and tonsils
2
Q
What product do pathogenic proteins produce?
A
bacterial toxins
3
Q
What product do pathogenic small particles produce?
A
Viruses
4
Q
What are the 6 fundamental immune responses against pathogens?
A
- Neutralisation of viruses and bacterial toxins by plasma proteins
- Ingestion & killing of pathogens by leucocytes (phagocytosis)
- Lysis of infected cells (cytotoxicity)
- Humoral response (complement + antibody)
- Containment of infected cells (granulomas)
- Cytotoxic lymphocytes
5
Q
What cells are used in eliciting the innate immune response?
A
Cells used in the Innate Immune Response
- Mast Cells
- Dendritic Cells
- Marcophages
- γδT-cells
- Natural Killer Cells
- Basophils
- Eosinophils*
- Compliment protein*
- Neutrophil*
* all are granulocytes
6
Q
What cells are used in the Adaptive Immune Response? (Be Specific)
A
Cells used in the Adaptive Immune Response
- B-cells = specifically the antibodies
- γδT-cells
- Natural Killer T-Cells
- T cells = specifically CD4+ & CD8+ (Thelper & Cytotoxic T cells)
7
Q
What cells are used in both the Innate and Adaptive Immune Responses?
A
- Natural Killer T cells
- γδTcells
8
Q
What are the differences between the Innate and Adaptive Immune Responses? (hint = should be 7 differences)
A
Innate
Adaptive
Naturally present
Produced after exposure to antigens
Present at birth
Develops during childhood
Rapid onset (hours to days)
Slow onset (days to weeks)
No specificity
Antigen specificity
No memory
Memory for antigens (B and T cells)
Limited diversity
High Diversity
Present in invertebrates and vertebrates
Present in vertebrates only
9
Q
What is the humoral Immune response?
A
Humoral Immune Response
Innate & Adaptive immune responses mediated by soluble (cell-free) proteins in the plasma, interstitial fluids and mucosal secretions
10
Q
What is the cellular immune response?
A
Cellular Immune Response
Is the innate and adaptive immune responses mediated by cells of the immune system (particularly effective against intracellular pathogens)
11
Q
Label the diagram
A
The Complement System
- Lyse Bacterial by forming MAC
- Tag Pathogens to enhance recognition and destruction by phagocytes opsonisation)
- Active inflammatory response by triggering the release of histamine from mast cells
- Enhance clearance of antigen-antibody complexes
A = Lysis
B = MAC = Membrane Attack Complex
C = Target Cell
D = Opsonization
E = Bacteria
E 2.0 = Phagocyte
F =Activation of inflammatory response
G =Complement Receptor
H = Extravasation
I = Mast Cell
J = Degranulation
K = Tissue
L = Blood
M = Clearance of immune complexes
N = Ag-Ab complex
O = Phagocyte
12
Q
What are the different types of antigens in placental animals (i.e. Humans, sheep etc.)?
A
Immunoglobin types
- IgM
- IgD
- IgE
- IgG
- IgA
13
Q
What the different types of immunoglobin types in birds?
A
Immunoglobin Types
- IgM
- IgY (with 2 different shapes)
- IgA
14
Q
What are the different types of immunoglobin present in Amphibians?
A
Immunoglobin types
- IgM
- IgY (1 shape)
- IgX
15
Q
What are the different types of immunoglobins present in bony fish?
A
Immunoglobin types
- IgM
- IgO
16
Q
What are the different types of immunoglobins present in cartilaginous fish?
A
Immunoglobin Types
- IgM
- IgW (two different shapes)
- IgNAR
17
Q
What are the different types of immunoglobins present in jawless fish?
A
hahah trick question they have none
18
Q
Of the different classes of vertebral animals which are positive or negative to …
a. having DNA rearrangment, hypermutation & a thymus and spleen
b. Class switch
c. Germinal centre formation
(Classes are; 1 = placental mammals, 2 = birds, 3 = amphibians, 4 = Bony fish, 5 = Catilaginous fish & 6 = Jawless fish)
A
- Placental mammals
- a. +ive
- b. =+ive
- c. +ive
- Birds
- a. +ive
- b. +ive
- c. +ive
- Amphibians
- a. +ive
- b. +ive
- c. -ive
- Bony Fish
- a. +ive
- b. -ive
- c. -ive
- Cartilagous fish
- a. +ive
- b. -ive
- c. -ive
- Jawless fish
- a. ???
- b. -ive
- c. -ive
19
Q
What do naive mature B-cells differentiate into?
A
a. Plasma Cells
b. Memory B cells
20
Q
What is the function of plasma Cells?
A
Plasma Cells
- produces or secretes IgG, IgA, IgE but requires the help of T cells
- IgM can be produced by B cells independently of help from T cells
21
Q
What is the function of memory B cells? What is the difference between long and short lived memory B cells?
A
Memory B cells
- express antibodies on their surface
- do not produce antibodies until a MAC or Ab-Ag complex is formed
- long lived memory B cells produce IgG, IgA or IgE but require help from the T cells
- short lived memory B cells only produce IgM (no T cell help)
22
Q
What are the different types of cells in the formation of both memory B & plasma cells? (does the cell have any extra things? i.e. any antibodies)
A
- Stem Cell
- Progenitor B-cell
- B-cell Precursor
- Immature B = IgM antibodies
- Mature B = IgM & IgD and the first or primary antigen is presented to the cell
- Either forms
- a. Memory B cell
- b. plasma cell which has either IgM or (if T cell helps) IgG, IgA or IgE
- On second exposure to antigen the memory B cells act on plasma cells to elicit an immune response
23
Q
What is the function of IgD immunoglobins?
A
IgD
- are produced by mature B cells
- fuse with the membrane during the exocytosis of the IgD antibody
- Are a primary B cell receptor
24
Q
What is the function of the IgM immunoglobulin?
A
IgM
- is either monomeric or pentamer
- is one of the primary B cell receptors
- Are secreted by the Plasma Cells
- secreted in both the primary and second immune responses BUT higher % in primary
- Activate the complement complex (MAC) & opsonophagocytosis
- Cause agglutination
25
why is it problematic if a person is given the wrong blood type? What is the cause of this?
Agglutination of blood
* As blood presents antibodies on its surface
* If the wrong blood is given IgM will bind to it
* stimulates agglutination of blood = clot
* known as type II hypersensitivity
26
What are the different isotypes of IgG immunoglobulin? What are their functions?
IgG isotypes
1. IgG1
* Broad complement and causes cell activation
2. IgG2
* Activates opsonophagocytosis of the antigen complex
3. IgG3
* Broad complement and causes cell activation
4. IgG4
* Unclear, May regulate antibody activity
27
In general, what is the function of the IgG immunoglobulins?
IgG immunoglobin
* is most abundant antibody found in the plasma
* Is produced in both primary and secondary immune responses but predominately in the second
* activation of MAC, opsonophagocytosis, neutralisation or triggers inflammation
28
What happens when a bacteria bind to the IgG antibody?
Causes the activation of the complement system which activates;
* MAC = Membrane Attack Complex
* Opsonisation
* C3 or C5A which causes inflammation
29
What happens when a viral body binds to an IgG antibody?
Renders the viral body inactive through NEUTRALISATION which means the virus cannot enter or bind to a cell
30
What happens when a free antigen binds to an IgG immunoglobin?
When the antigen and antibody bind will cause the antigen to precipitate.
which activates; opsonisation & phagocytosis
Process called **Precipitation**
31
In general, what is the function of IgA immunoglobulins? Where is it found?
IgA
* is a dimer
* found in mucosal tissue areas like saliva, skin secretions, mucosal lining of GIT, milk from lactation & urogenital tract
* Loves to destroy bacteria in the above areas
* works in the same mechanisms as IgG
32
What are the different isotypes of IgA and what are their specific function?
IgA
a. is a mucosal antibody
b. is a specific mucosal antibody to proteolytic bacteria
33
What is the function of the IgE immunoglobulin? Where are they found?
IgE immunoglobins
* are monomers secreted by plasma cells
* found in; respiratory tract mucosa, urogenital structures, lamina propria and lymphatic tissues
* activates mast cells and eosinophils
* Bind to the FcεR1 on Mast Cells during inflammation
* when a person is exposed to an allergen
* causes the release of histamine, interleukins, prostaglandins etc.
* causes vasodilation and increases the permeability of blood vessels
* Can also be activated when you have a parasitic worm
34
What are the Effects of antibodies to pathogenic microbes?
1. Neutralisation of bacterial toxins and viruses
2. Opsonisation of particles for phagocytosis by cells with various effect functions.
* Cells include = Neutrophils, monocytes/macrophages, conventional & plasmacytoid dendritic cells
3. Activation of the complement pathway
4. activation of NK cells antibody-dependant cell-mediated cytotoxicity (ADCC)
5. Activation of basophils/mast cells
6. Activation of eosinophils
35
What disease do each of the following toxin-producing bacteria cause?
1. Clostridium tetani
2. Staphylococcus aureus
3. Bacillus anthracis
4. Bordetella pertussis
5. Corynebacterium diptheriae
1. Tetanus
2. some manifestation of staphylococcal disease
3. Anthrax
4. Whooping Cough
5. Diphtheria
36
What toxin-producing bacteria is the cause of the following diseases?
1. Tetanus
2. Some manifestations of Staphlococcal disease
3. Anthrax
4. Whooping Cough
5. Diphtheria
1. Clostridium tetani
2. Staphylococcus aureus
3. Bacillus anthracis
4. Bordetella pertussis
5. Corynebacterium diptheriae
37
Describe the process of neutralisation.
NEUTRALISATION
a toxin (or antigen) binds to the toxin receptor of host cell
the formation of the Ag-Ab complex causes the precipitation of the complex
This results in it being rendered inactive or neutralised
38
Describe the process of phagocytosis of a particular antigen. (7 steps)
Phagocytosis of an antigen
1. Adherence of microbe to phagocyte
2. ingestion of microbe by the phagocyte
3. Formation of phagosome
4. Fusion of phagosome with lysosome = phagolysosome
5. digestion of microbe by enzymes
6. formation of residual bodies containing ingestible material
7. discharge of waste
39
How do phagocytes trigger inflammation?
Through activation of multiple cell surface molecules in apoptotic, gram +ive, gram -ive and yeast cells
40
What are the types of phagocytes that can cause opsonisation and phagocytosis and describe the process of opsonisation & phagocytosis?
Phagocytes
* neutrophils
* monocytes
* Macrophages
* Dendritic Cells (conventional & plasmacytoid)
Process of opsonisation & phagocytosis
1. opsonins bind to the surface of the antigen so it can be recognised by the phagocyte. Makes the antigen PALATABLE.
2. The opsonised antigen binds to the Fc & C3b receptors of the phagocyte where it is digested by the phagocyte
41
What are the functional phagocytic effects of neutrophils?
Intracellular killings (of bacteria and fungi)
42
What are the functional phagocytic effects of monocytes/macrophages?
Antigen processing and presentation to B and T lymphocytes
Intracellular killing (of bacteria, mycobacteria and fungi)
43
What are the functional phagocytic effects of Conventional dendritic cells?
Antigen process and presentation to B and T lymphocytes
44
What are the functional phagocytic effects of Plasmacytoid dendritic cells?
Production of types 1 interferons (which are signalling molecules)
45
What is the difference between conventional and plasmacytoid dendritic cells?
Conventional
* are similar to monocytes
* two subset cDC-1 & cDC-2
* produce IL-12, IL-6, TNF & chemokines
Plasmacytoid
* resemble plasma cells
* produce interferon-α
46
Describe the process of antibody-dependant cell-mediated cytotoxicity (ADCC) & state which cells perform this process.
**Antibody-dependant cell-mediated cytotoxicity (ADCC)**
* is performed by NK cells
1. An antibody-coated cell with surface antigens binds to an IgG antibody
2. This forms an antibody-antigen complex
3. An NK T-cell has a FcγRIII which binds to the complex as it has a low affinity to the antigen-antibody complex.
4. Results in the killing of the antibody-coated cell
47
Describe how the activation of Eosinophils occurs when a helminth parasite is around.
1. IgE antibodies bind to Fab receptors on the helminth
2. As the IgE antibodies have a Fc receptor which then causes an eosinophil to bind to it (& thus, the helminth)
3. This causes the release of lysosomes into the helminth
4. The lysosomes release their contents into the helminth which results in its digestion
48
What are the different effects of Mast cell Activation? (hint there are 9)
Some of the effects of Mast Cell Activation
1. Lymphocyte retention
2. Contraction of smooth muscle
3. Sensation of Pain
4. Cytokine and mucus production
5. Activation of macrophages and intracellular killing
6. Antigen presentation in dendritic cells
7. Chemotaxis & bacterial killing (neutrophils)
8. Upregulation of adhesion molecules and vascular permeability
9. T-cell chemotaxis and activation
49
How do Mast cells cause an effect on lymphocyte retention?
* through lymphocyte retention in draining lymph nodes and enhanced antibody production by the B-cells.
* causes the release of IgG and IgE antibodies to be released
* They bind to the FcεR1 receptors on the Mast cell which increases lymphocyte retention
*
50
How do Mast cells cause an effect on the contraction of smooth muscle?
Mast cells can cause the contraction of smooth muscle through eicosanoids (i.e. LTC4 & LTD4)
51
How do Mast cells cause an effect on Pain?
Mast cells have an effect on pain through eicosanoids (i.e. PGI2 & PGE2) or substance P
52
How do Mast cells cause an effect on Mucus & cytokine production?
Mast cells act on mucus-producing epithelial cells which causes increase secretion of mucus & cytokines
53
How do Mast cells cause an effect on the activation of macrophages and intracellular killing?
Mast cells through the release of e.g. IL-4 causes the activation of macrophages & therefore intracellular killing
54
How do Mast cells cause an effect on Antigen presentation of dendritic cells?
Mast cells release TNF & histamine which causes the dendritic cells to present antigens on their surface as well as causes their recruitment into specific tissue & mobilisation to drain into lymph nodes
55
How do Mast cells cause an effect on Chemotaxis & bacterial killing?
Mast cells act on neutrophils through TNF, Proteases (i.e. MCP1) & IL-6 which cause their chemotaxis to a site of injury. This also stimulates the neutrophils to travel to toxin-producing bacteria and then kill that bacteria
56
How do Mast cells cause an effect on endothelial cells? (hint = 2 ways they act on them & where are endothelial cells present)
Mast cells act on endothelial cells through;
* TNF, eicosinoids (i.e. LTB4)
* Activation of neutrophils (thru TNF, Proteases & IL-6)
Which cause the upregulation of adhesion molecules & has an effect on the vascular permeability of those endothelial cells
57
How do Mast cells cause an effect on T-cells?
Mast cells act on T-cells through many different chemicals e.g. CCL5
this causes the activation of the T-cell through antigen presentation & T-cell chemotaxis
58
What is Chemotaxis?
Is the movement of an organism (somatic cell, bacteria or another single-celled organism) in response to a chemical stimulus. Can cause the organism to be repelled from an area or be "drawn" to an area
59
Why does mycobacterium tuberculosis evade killing even though it is phagocytosed?
1. The macrophage attaches to mycobacterium tuberculosis as the cell membrane surrounds the cell
2. mycobacterium tuberculosis is now internalised in a phagosome
3. the lysosome fuses with the phagosome to form a phagolysosome
4. the phagolysosome as mycobacterium tuberculosis reduces the acidity of contents of the phagolysosome
5. This results in it evading killing and eventually will take control over that cells from the inside
60
Why do *Mycobacterium tuberculosis (MTB)-*infected macrophages can be activated by T-cells?
1. As the MTB is kept within the cell (aka the cell hasn't been able to apoptosis or kill the MTB)
2. The MTB-infected macrophage still functions normally & due to its hijacking produces IL-23 & IL-12
3. IL-23 & IL-12 act on IL- receptors on the T-cell which cause it to produce an IFN-γ
4. IFN-γ causes increase phagocytic effects
5. Causes more cells to come to infected cell = granuloma = more cells infected
61
How do cytolytic lymphocytes kill virus-infected cells or tumour cells?
In a healthy cell;
* the TCR of the cytolytic lymphocyte does not bind to the HLA class 1 + self-peptide
* no activation of HLA-1 & TCR
* results in the expression of an inhibitor receptor which prevents the NK cell inducing apoptosis
In an Unhealthy cell;
* The TCR of the cytolytic lymphocyte binds to the "self-peptide" in the HLA-1 receptor
* causes activation of the HLA-1 & TCR
* Results in the regression of the inhibitor receptor on the cells surface
* Allows the activating receptor to bind to the cell's membrane
* activates apoptosis of the cell as it is recognised as not self
62
What are the 2 "main" types of T-cells?
1. CD4+ T cells
* are T-helper cells
* use an exogenous pathway for antigen processing
* Are MHC-class II
2. CD8+ T cells
* are cytotoxic T cells (killer T cells)
* use an endogenous pathway for antigen processing
* Are MHC-class I
63
What are the difference between endogenous and exogenous antigen processing pathways?
Endogenous Pathway
* Used to present cellular peptide fragments on the cell surface of HMC - class I cells
* the antigens are found within the cytosol of cells (e.g. viruses and intracellular bacteria)
Exogenous Pathway
* is utelised by antigen-presenting cells to present peptides from proteins that have been endocytosis
* Presented on HMC class - II
* Proteins are endocytosed and degraded by acid-dependent proteases in endosomes; this process takes about an hour.
64
Where do T precursor cells mature?
T cells mature in the thymus
65
Describe the process of how they mature & what cells form?
T Precursor Cells have a TCR, CD8+ & CD4+ receptors present on its cells.
1. Positive Selection
* if one of the CD8+ or CD4+ receptors perfectly binds to either the HLA-Class 1 or the HLA-Class II receptor (of the thymus epithelial cells) respectively
* CD8+ CAN ONLY BIND TO HLA-Class 1
* CD4+ CAN ONLY BIND TO HLA-Class 2
* then the cell increases transcription for that receptor (CD8 or CD4)
* if it binds to neither = thymic cells secrete FAS which causes the cell to apoptose
2. Negative Selection
* If the TCR on the T-cell bind to the MHC self-peptide then the cell cannot different from its self
* FAS is secreted by the thymic cells and is secreted into the T cell = causes it to undergo apoptosis
* If the TCR DOES NOT bind to the self-peptide then it can recognise self from not self and is now mature
This process produces T-helper cells (CD4+) and Cytotoxic T cells (CD8+)
66
What are the main lymphoid organs and state if they are primary or secondary?
Lymphoid organs
1. Gut-Associated Lymphoid Tissue (secondary)
2. Thymus (primary)
3. Spleen (secondary)
4. Bone Marrow (primary)
5. Lymph Nodes (secondary)
6. Germinal Centres (secondary)
7. Peyer's Patches (secondary)
8. Appendix (secondary)
67
Where are Peyer's patches located?
in the small intestine specifically in the ileum
68
What are Germinal Centres? What is their function?
Germinal Centres are areas in secondary lymphoid organs - specifically spleen and lymph nodes, where the mature B cells proliferate, differentiate and mutate their antibodies
69
What are the different areas of mucosa-associated lymphoid tissue? (If possible specify the specific parts)
1. Intranasal (NALT)
* upper respiratory tracts
* lower respiratory tract
* genital tracts
2. Sublingual
* Upper respiratory
* lower respiratory
* gastrointestinal tract
3. Oral
* Gastrointestinal tract
* Salivary glands
* mammary glands
4. Rectal
* Rectal tract
* Genital Tract
5. Intravaginal
* Genital tract
70
What do NALT, BALT, GALT mean? What do they include?
* NALT = Nasal-associated lymphoid tissue
* Salivary glands & cervical lymph nodes
* more specifically Tonsils and adenoids
* BALT = Bronchiole-associated lymphoid tissue
* Bronchioles
* GALT = Gastric-associated lymphoid tissue
* Mesenteric lymph nodes
* Isolated lymphoid follicles
* Peyer's Patches
71
What specific organs are included in the Genital associated lymphoid tissue?
* inguinal lymph nodes
* para-aortic lymph nodes
72
Finish the diagram
73
What is the difference between the primary and secondary immune responses?
1. Primary Immune Response
* mainly produces IgM antibodies
* antibody concentration is lower
* takes longer to overcome
2. Secondary
* through immune memory is more rapid and causes a large immune response
* mainly IgG antibodies produced
* Quicker recover with less symptoms
74
How do immunisations utilise the primary and secondary immune responses?
Vaccines introduces an antigen or antibody to the immune system which results in a primary exposure to the antigen
75
What is a granuloma a sign of?
a granuloma is a sign of chronic inflammation
76
How do T(follicular)helper cells (Tfh) help the B cells? and Where does this occur?
Tfollicular regulator (TFR) Cells release IL-10 which then acts on the TFH Cells express the CXCR5 receptor which causes the release of CXCL 13 & IL-21
CXCL13 = helps B cells migrate to the germinal centres
IL-21 = causes the B cell to form memory B cells & plasma cells
Occurs in the lymph nodes & spleen
77
How do Treg Cells cause the inhibition of the Effector T cell?
* The Treg cell have membrane-tethered TGFβ (transforming growth factor)
* And to inhibit the effector cell releases;
* TGFβ
* inhibitory cytokines IL-35, IL-10
* Causes the inhibition of the effector T cell
78
How do Treg cells perform cytolysis?
* Treg cells release granzyme A or B
* Which enter the effector T cell through the perforin pores
* cause an apoptotic effect on the cell
79
How do Treg Cells cause metabolic disruption?
Works in 3 methods (i think)
1. **cAMP-mediated inhibition =** cAMP travels from the Treg Cells to the effector T cell through gap junctions and cause
2. **high-affinity CD25-dependant cytokine-deprivation-mediated apoptosis =** CD25 is also known as an IL-2α receptor which causes the effector T cell to die due to cytokine deprivation
3. **CD39-&/or CD73-generated, Adenosine receptor 2A-mediated immunosuppression** = Adenosine is released from the CD39 and/or CD73 & binds to the A2AR on the effector cell which causes it to be suppressed
80
How do Treg Cell target to dendritic cells?
Works in two ways
1. lymphocyte-activation gene 3-MHC-class-II-mediated suppression of DC maturation
2. cytotoxic T-lymphocyte antigen-4-CD80/CD86-mediated induction of indoleamine-2,3-dioxygenase
Cause cell to die
81
What are the four basic mechanisms used by Treg cells?
1. Inhibitory cytokines
2. Cytolysis
3. Metabolic disruption
4. Targeting dendritic cells
82
How do CD4+ T cells help CD8+ T cells?
CD4+ T cells act on CD8+ T cells and cause the release of cytokines, chemokines and other chemicals which cause the lysis of infected cells
83
If a person has CD4+ T helper cells, what is this an indicator of?
Is an indication that the person has been exposed to a disease or virus at least 6 months ago
84
How do T cell generate a response? (generally speaking)
* An infectious agent activates a dendritic cell which travels to the lymphatic system
* Activates a Naive T cell & causes it to present a specific antigen
* The specific antigen acts on the infected cell through the viral-peptide present in the MHC class 1 receptor on its cell surface
85
What are the different layers of tolerance mechanisms?
1. Central Tolerance
2. Antigen Segregation
3. Peripheral anergy
4. Regulatory cells
5. Cytokine deviation
6. Clonal deletion
86
What is the mechanism & site of action of Central tolerance?
* Mechanism
* Deletion & Editing
* Site of Action
* Thymus & Bone marrow
87
What is the mechanism & site of action of Antigen segregation?
* Mechanism
* Physical barrier to antigen access to lymphoid
* Site of Action
* Secondary lymphoid organs
88
What is the mechanism & site of action of Periphery Anergy?
* Mechanism
* Cellular inactivation by weak signalling without co-stimulus
* Site of Action
* Secondary lymphoid tissue and sites of inflammation
89
What is the mechanism & site of action of Regulatory Cells?
* Mechanism
* suppression by cytokines, intracellular signalling
* Site of Action
* secondary lymphoid tissue & sites of inflammation
90
What is the mechanism & site of action of Cytokine Deprivation?
* Mechanism
* Differentiation to TH2 cells limiting inflammatory cytokine secretion
* Site of Action
* secondary lymphoid tissue and sites of inflammation
91
What is the mechanism & site of action of Clonal deletion?
* Mechanism
* Apoptosis post-activation
* Site of Action
* secondary lymphoid tissue & sites of inflammation
92
Labe the diagram
1. Lymphoid Precursor
2. Self Antigen (Ag) in Bone Marrow or Thymus
3. Deletion of high-affinity self Ag lymphocytes
4. Maturation of clones weakly responsive to self Ag
5. Foreign Ag
6. Immune response to foreign Ag
7. Self Ag in peripheral tissues
8. Regulation or energy of self Ag Specific lymphocytes
93
What is hypersensitivity?
Are disorders in the adaptive immune response which cause the host to have impaired defence against microbial infections which result in tissue injury & diseases
94
What are the different types of hypersensitivity?
1. Type I = IgE-mediated hypersensitivity
2. Type II = IgG-mediated cytotoxic hypersensitivity
3. Type III = Immune Complex-mediated hypersensitivity
4. Type IV = Cell-mediate hypersensitivity (delayed)
95
Briefly describe Type I hypersensitivity.
* IgE mediated
* immediate hypersensitivity = 30 mins after exposure
*
96
Briefly describe Type II hypersensitivity.
* IgG or IgM mediated
* is cytolytic or cytotoxic
*
97
Briefly describe Type III hypersensitivity.
* mediated when immune complexes (Ag-IgM or Ag-IgG) activated complement
* complement is then precipitated
* Granulocytes (e.g. neutrophils) are attracted to the site of activation
* damage is caused by the release of lytic enzymes
* Reaction occurs within hours of challenge with antigen
98
Briefly describe Type IV hypersensitivity.
* involves both cytotoxic & TH1 cells
* is mediated by TH1 cells & when activated;
* releases Cytokines = accumulation of macrophages
* activation of cytotoxic T cells = local damage
* Reaction occurs weeks after antigen
99
