Immunology Flashcards
1
Q
what is vaccination
A
the DELIBERATE exposure to an antigen to induce immunologically-mediated resistance to the disease through the induction memory
2
Q
what is immunisation
A
the process through which an individual develops immunity/memory to a disease
3
Q
what types of immunity are there
A
passive and active
4
Q
what is active immunity
A
protection against a disease produced by the body’s OWN immune system
5
Q
how long does active immunity last
A
usually permanent
6
Q
give examples of methods of gaining active immunity
A
vaccination, via infection
7
Q
what is passive immunity
A
protection against a disease TRANSFERRED from another person or animal
8
Q
give examples of methods of gaining passive immunity
A
breast milk (IgA) placental transfer (IgG)
9
Q
what cells are involved in production of memory
A
memory B and T cells
memory CTLs
long-lived plasma cells
10
Q
what type of T cell is involved in producing memory
A
CD4+
11
Q
what is needed for memory to be produced (______ & _____ of the immune system)
A
stimulation & maturation of the immune system AFTER exposure to antigen
12
Q
what cells are involved in the PRIMARY adaptive immune response
A
T and B cells
13
Q
in what state do T and B memory cells survive in the body and for how long
A
dormant for years
14
Q
how do T and B cells reactivate
A
rapidly
clonal proliferation + expansion then the differentiate into effector cells or memory cells
15
Q
what have B memory cells already undergone
A
Ig class switching and hypermutation
16
Q
what properties of T and B memory cells have been enhanced
A
cell adhesion and chemotaxis
17
Q
compare active vaccination to memory generated by natural infection
A
immune response is stimulated in the SAME way
18
Q
what types of active vaccination are there
A
live attenuated
inactive
19
Q
describe the features of inactive vaccines
A
can’t replicate inside the host
requires multiple doses
20
Q
what is the response to inactive vaccines
A
ANTIBODY bases (not T cells)
21
Q
describe the features of live attenuated vaccines
A
very effective
single dose
may cause infection immunocompromised host
22
Q
what infections can vaccine NOT be developed for
A
chronic/latent infections (e.g HIV, Herpes, Hep C)
rapidly evolving infections (e.g. HIV, flu)
23
Q
what are adjuvants
A
mixtures of inflammatory substances required to stimulate immune responses to co-administered vaccine
24
Q
what are the hallmarks of immune deficiency
A
(SPUR)
Serious infections
Persistent infections
Unusual infections
Recurrent infections
25
what counts as a serious infection
unresponsive to ORAL antibiotics
26
what counts as an unusual infections
unusual organism and/or site
27
what counts as a recurrent infection
2 major infection OR 1 major and 1 minor infections in one year
28
how are immunodeficiencies
secondary and primary
29
compare primary and secondary immunodeficiencies
secondary is common, subtle and often involves more than 1 component of the immune system
primary is rare with a strong family history
30
give examples of causes of secondary immunodeficiencies
```
extremes of life
infection (HIV, measles)
treatment (steroids, chemo, immunosuppressants)
cancer
malnutrition
renal insufficiency/dialysis
diabetes (type 1 + 2)
```
31
innate immune system immunodeficiencies involve what cells
phagocytes (neutrophils + macrophages)
32
what are the 5 steps in a phagocyte life cycle
1. Mobilisation from bone marrow or within tissues
2. adhesion and migration into tissues
3. Recognition of the organism
4. Phagocytosis and killing of organism
5. Activation of other components of immune system
33
what NORMALLY happens during the 1st step of phagocyte life cycle
stem cells differentiate then mature before leaving the bone marrow
34
what NORMALLY happens during the 2nd step of phagocyte life cycle
up regulation of endothelial adhesion markers (selections & intergrins) allow transendothelial migration
35
what NORMALLY happens during the 3rd step of phagocyte life cycle
recognition of organism via PRR:PAMP (direct) OR opsonins (indirect)
36
what NORMALLY happens during the 4th step of phagocyte life cycle
killing happens after engulfment when free radicals are released via an oxidative burst
37
what NORMALLY happens during the 5th step of phagocyte life cycle
macrophages secrete IL-12 which induces TH1 to secrete INF-gama which feedbacks to the phagocyte stimulating the oxidative pathway (free radicals)
38
what can go wrong during the 1st step of the phagocyte life cycle (2 ways)
1. failure to DIFFERENTIATE = reticular dysgenesis which results in infant death
2. failure to MATURE = kostmann syndrome (NO neutrophils)
39
what can go wrong during the 2nd step of the phagocyte life cycle
failure to recognise activation markers on endothelial cells = leukocyte adhesion deficiency
40
what does leukocyte adhesion deficiency result in
neutrophils CANNOT EXIT the bloodstream leading to high levels within the blood but NONE in the tissues
41
what can go wrong during the 3rd step of the phagocyte life cycle
defect in RECOGNITION or OPSONIN = less affective phagocytosis
42
what does issues in the 3rd step of the phagocyte life cycle result in
no significant disease
43
what can go wrong during the 4th step of the phagocyte life cycle
failure of the oxidative killing mechanism resulting in chronic granulomatous disease
44
what is chronic granulomatous disease
inability to generate O2 free radicals (ROS/RNS)
45
How is hronic granulomatous disease diagnosed
via NBT test
46
what can go wrong during the 5th step of the phagocyte life cycle (3)
1. INF-gamma receptor deficiency
2. IL-12 deficiency
3. IL-12 receptor deficiency
47
what is autoimmunity
presence of immune responses to self-tissues/cells
48
what are the 3 main causes of autoimmune disease
immune regulation
environment
gene
49
how does immune regulation result in autoimmune disease
it is responsible for maintaining self tolerance
50
how does environment result in autoimmune disease
molecular mimicry
51
what is molecular mimicry
cross-reactivity between antigens expressed by pathogens and self, usually caused by infection
52
how do genes result in autoimmune disease (2 types)
monogenic disorders
| complex genetic interplay
53
give an example of a monogenic autoimmune disorder
IPEX Syndrome
54
what is IPEX Syndrome
failure of peripheral tolerance due to defective regulatory T cells
55
give an example of complex genetic interplay autoimmune disorder
HLA genes
56
what are HLA genes
associated with but not a prerequisite for autoimmune disease
57
describe what tolerance is and why it is required
some T cells mutate to recognise self and foreign, tolerance mechanisms ensure these cells are eliminated before they are able to mature and harm self
58
give examples of type 1 autoimmune conditions (Gel Coombs classification)
none
59
give examples of type 2 autoimmune conditions (Gel Coombs classification)
Grave's disease
| Goodpasture's syndrome
60
give examples of type 3 autoimmune conditions (Gel Coombs classification)
SLE (lupus)
61
give examples of type 4 autoimmune conditions (Gel Coombs classification)
type 1 diabetes
coeliac disease
Rh arthritis
62
what is a hypersensitivity reaction
immune response that results in bystander damage to self
63
what is a hypersensitivity reaction an exaggeration of
normal immune mechanisms
64
what is type 1 hypersensitivity reaction
immediate hypersensitivity (allergy)
65
what is type 1 hypersensitivity reaction characterised by
enhanced sensitivity to normally innocuous substances leading to physiological damage
66
what Ig_ is involved in type 1 hypersensitivity reaction
IgE
67
what is an allergy
IgE-mediated response to an external antigen (allergen)
68
what are the clinical features of a type 1 hypersensitivity reactions
occurs quickly (mins- 1 or 2 hrs)
presentation depends on site of contact
rash, angiodema,anaphylaxis
69
what immune cells are involved in type 1 hypersensitivity reactions (3)
B cells
T cells
Mast cells
70
what is the role of B cells in type 1 hypersensitivity reactions
recognises antigen and produces SPECIFIC IgE antibodies
71
what is the role of T cells in type 1 hypersensitivity reactions
helps B cells to produce antibodies
72
what T cells are involved type 1 hypersensitivity reactions
Th2
73
what is the role of mast cells in type 1 hypersensitivity reactions
express receptors for the Fc region of the IgE antibody, residual antibodies will remain even after the antigen is cleared. if the allergen is re-encountered it will bind to the IgE coated surface, disrupting the membrane and causing the release of vasoactive substances
74
give an example of an type 1 hypersensitivity reactions
asthma, hay fever, allergic rhinitis
75
what is he gold standard test for allergy
skin prick test
76
give the management options of allergy (5)
```
targeted avoidance
sodium cromoglycate
antihistamines
leukotriene receptor agonist
corticosteroids
```
77
what is the role of sodium cromoglycate in the treatment of allergy
mast cell stabilisers
78
what is an type 2 hypersensitivity reaction
direct cell killing due to cell bound antigen
79
what is type 2 hypersensitivity reactions also known as
antibody dependent hypersensitivity
80
what causes type 2 hypersensitivity reactions
IgM or IgG binding to a self antigen or a foreign antigen which is attached to a human cell
81
what cells are involved in an type 2 hypersensitivity reaction
B cell
| IgM or IgG
82
what antibodies are involved in type 2 hypersensitivity reaction
IgM
| IgG
83
what does the bound antibody interact with in an type 2 hypersensitivity reaction, what does these interacts result in
complement or the Fc receptor on macrophages
activation of complement (causing cell lysis + opsonisation)
opsonisation (antibody mediated phagocytosis)
84
what is the management of type 2 hypersensitivity reactions
plasmapheresis
| immunosuppression
85
give examples of type 2 hypersensitivity reactions
immune haemolytic anaemias
86
give examples of immune haemolytic anaemias
drug induced haemolysis
| acute haemolytic transfusion reaction
87
what is type 3 hypersensitivity reaction
immune complex mediated
88
describe what happens during a type 3 hypersensitivity reaction
immune complexes which are trapped within the body attract inflammatory cells which cause damage to the body
89
what cell are involved in a type 3 hypersensitivity reaction
B cells
IgG
neutrophils
90
what Ig_ is involved in a type 3 hypersensitivity reaction
IgG
91
what causes immune complexes to form
in the presence of excess antigen, antibodies will bind together to form immune complexes
92
what is the management of type 3 hypersensitivity reactions (3)
```
avoidance
decrease inflammation (corticosteroids)
decrease antibody production (immunosuppression)
```
93
Give an example of type 3 hypersensitivity reactions
Hypersensitivity pneumonitis (______ lung)
94
what is type 4 hypersensitivity reactions
delayed
95
what mediates type 4 hypersensitivity reactions
T cells.
96
what cells are involved type 4 hypersensitivity reactions
Th1 cells
| macrophages
97
explain what happens during a type 4 hypersensitivity reaction
initial exposure to the antigen results in the generation of "primed" Th1cells. subsequent exposure activated "primed" cells which recruit macrophages
98
give examples of type 4 hypersensitivity reaction (4)
autoimmune
. type 1 diabetes
. rheumatoid arthritis
non-autoimmune
. contact dermatitis (e.g. poison ivy)
. sarcoidosis
