Immunology Flashcards

1
Q

Innate Immunity

A

Natural immunity that is present from birth and is generally non-specific and fast

Includes physical barriers, inflammatory mediators, complement proteins, acute phase proteins, immune cells

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2
Q

What does the immune system do

A

identifies and eliminates microorganisms by distinguishing self molecules from non self molecules and identifying danger signals

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3
Q

ways to manipulate the immune system to prevent or treat human disease

A

immunisation
anti-inflammatory and immunosuppressive drugs
cancer immunotherapy

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4
Q

barriers to infection - skin

A

physical barrier - tightly packed, highly keratinised cells,

physiological factors - low pH (5.5), low oxygen tension

sebaceous glands - hydrophobic oils, lysozymes, ammonia

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5
Q

Tell me about mucus

A

Mucous membranes line all body cavities that are in contact with the external environment

Mucus traps bacteria and contains lysozymes and defensins that directly kill invading pathogens

Secretory IgA

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6
Q

tell me about commensal bacteria

A

Compete with pathogens for resources and produce fatty acids and bactericides that stop pathogens growing

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7
Q

What are cytokines

A

Interferons released by virally infected cells signal to neighbouring uninfected cells :

destroy RNA and reduce protein synthesis and undergo apoptosis

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8
Q

What do interferons activate

A

immune cells e.g. NK cells

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9
Q

What are acute phase proteins

A

Proteins produced by the liver whose plasma concentrations increase or decrease in response to inflammation

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10
Q

What are examples of acute phase protiens

A

C3 - complement system protein
MBL - complement system protein
CRP - activates complement via classical pathway

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11
Q

What is transendothelial migration

A

the recruitment of neutrophils to the site of infection/damage during acute inflammation

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12
Q

What are the stages of transendothelial migration

A
  1. Loss of intravascular fluid in the presence of inflammation causes slower blood flow, allowing neutrophils to undergo margination (neutrophils travel close to endothelial cells instead of centre of the vessel)
  2. Neutrophils can then encounter and bind to adhesion molecules expressed by the endothelial cells
  3. Neutrophils migrate across the endothelium via diapedesis
  4. Once in the tissues, the neutrophils travel to the exact site of injury via chemotaxis
  5. Neutrophils are then activated by PAMPs and pro-inflammatory mediators such as TNFa
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13
Q

What are types of killing mechanisms

A

NETs
Phagocytosis
Degranulation

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14
Q

Tell me about NETs

A

neutrophil extracellular traps : release of a net-like structure that traps pathogens, leading to phagocytosis

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15
Q

Tell me about phagocytosis

A

Pathogens release chemical signals that attract neutrophils, which use PRR to bind to and phagocytose these pathogens

Kills internalised pathogens via 2 distinct mechanisms : phagolysosomal killing and ROS-dependent killing

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16
Q

Tell me about degranulation

A

release of anti-bacterial granules leading to direct damage and systemic inflammation

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17
Q

What are the modes of ingestion

A

Receptor mediated endocytosis

Pinocytosis

Phagocytosis

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18
Q

Tell me about receptor mediated endocytosis

A

molecules bound to membrane receptors are internalised

important in the generation of adaptive immunity

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19
Q

Tell me about pinocytosis

A

ingestion of fluid of surrounding cells

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20
Q

Are macrophages a phagocytic cell

A

Yes

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21
Q

what is macrophages phagocytosing bacteria facilitated by

A

opsonization

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22
Q

What is opsonisation

A

the coating of pathogens by soluble factors (opsonins) to enhance phagocytosis

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23
Q

What are the stages of phagocytosis

A
  1. PRRs on macrophages bind to PAMPs on pathogen which signals the formation of the phagocytic cup
  2. Cup extends around the pathogen and pinches off - phagosome
  3. Phagosome fuses with lysosome - phagolysosome
  4. Pathogen killed and contents degranulated n
  5. Debris released into extracellular fluid
  6. Pathogen-derived peptides expressed on special cell surface receptors (MHC-II)
  7. Pro-inflammatory mediators released (TNFa) - acute inflammation
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23
Q

What are examples of opsonins

A

C3b
C-reactive protein (CRP)
IgG/IgM

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24
Are dendritic cells phagocytic cells
yes
25
What do dendritic cells do
act as a bridge between the innate and acquired immune system express antigens on their cell surface and present them to T cells
26
What are eosinophils associated with
allergy
27
Tell me about basophils
Granules contain histamine etc. act as effector cells in allergic reactions
28
What do mast cells deal with
pathogens too large for phagocytosis
29
What are mast cells associated with
Allergy
30
What is gene expression
Production of new pro-inflammatory substances e.g. leukotrienes and prostaglandins
31
What can immune systems be enhanced by
antibodies
32
What is acquired (adaptive immunity)
Immunity that is not present from birth Is specific and slow
33
What is acquired (adaptive) immunity induced by
foreign material
34
Is acquired immunity able to discriminate between self and non-self
Yes
35
What does acquired immunity include
cytokines, antibodies, B and T cells
36
The complement system, when activated, creates a cascade of chemical reactions that promotes:
opsonisation of pathogens direct pathogen killing accute inflammation leukocyte recruitment
37
Where are low levels of inactive complement system proteins normally found
plasma and extracellular fluids
38
Go and learn the complement system pathways
NOW!!!!
39
Where do B cells mature
in the bone marrow
40
What are B cells important in
humoural immune response
41
What do B cells produce
antibodies that attack pathogens circulating in the blood and lymph
42
B cells play a key role in defence against ...
extracellular pathogens
43
What do B and T cells normally circulate around
their primary lymphoid tissue (site of development) in their inactive form
44
What activates the B and T cells and where
Antigen presentation in the secondary lymphoid tissue (lymph nodes, spleen, MALT)
45
B cell activation : what do membrane-bound antibodies on the B cells bind to
target antigen IgM (or IgD)
46
Why are neutrophils much better killers than macrophages
Because they have a 2nd way to kill internalised pathogens
47
How many signals to B cells require to become fully active
2
48
Once activated, what do B cells become
plasma cell (antibodies) or a memory B cell
49
What is generated in B cell activation
IgM and IgG
50
Tell me about the transport of lymphocytes
Lymph and Lymphocytes leave lymph node, medullary sinus, efferent lymphatic vessels, blood circulation via lymphatic ducts at the subclavian vain
51
What is Ig
immunoglobin
52
What are antibodies made up of
2 light chains and 2 heavy chains
53
Where are membrane bound antibodies located
surface of B cell
54
what is agglutination
the action of an antibody when it cross-links multiple antigens producing clumps of antigens
55
what does agglutination do
enhance phagocytosis prevents viruses from binding to and infecting host cells
56
What is the first antibody to be made in an infection
IgM
57
When is IgM a monomer/pentamer
Monomer when bound to B cell membrane Pentamer when released into plasma
58
What are the functions of IgM
B cell activation, agglutination, complement system activation through classical pathway
59
What is the most abundant antibody in the plasma
IgG
60
Is IgG a monomer or pentamer
Monomer
61
What are the functions of IgG
foetal immunity (placental transfer)
62
What is the second most abundant antibody
IgA
63
What are the functions of IgA
neonatal defense (found in breastmilk)
64
What are IgE produced in
allergic response
65
Where to T cells mature
thymus
66
What can T cells recognise
peptide antigens
67
What are regulatory T cells involves in
lymphocyte suppression
68
What are memory T cells involved in
the adaptive immune response
69
Tell me about CD4+ Helper T cells
activate B cells and stimulate production of memory B cells
70
Tell me about CD8+ killer T cells
kill infected cells
71
What can T cells only recognise
peptide antigens that are presented to their TCR by MHC molecules
72
Tell me about Class I MHC
expressed on all nucleated cells present peptide antigens to CD8+ killer T cells
73
Tell me about Class II MHC
expressed only on antigen presenting cells (e.g. dendrites, macrophages), present peptide antigens to CD4+ helper T cells
74
What are hypersensitivity reactions
Immune response that results in bystander damage to the self usually exaggeration of normal immune mechanisms
75
Type 1 hypersensitivity reaction
immediate hypersensitivity
76
Type 2 hypersensitivity reaction
direct cell effects
77
Type 3 hypersensitivity reaction
immune complex mediated
78
Type 4 hypersensitivity reaction
delayed type hypersensitivity
79
Are most complex diseases one or a combination of the types of hypersensitivity
combination
80
what is a classical type of type 1 hypersensitivity (immediate)
allergy, mediated by the inappropriate production of specific IgE antibodies to harmless antigens
81
What are the cells involved in type I hypersensitivity reactions
Mast Cells, B Cells, Eosinophils
82
Children who produce more Th2 ...
are more likely to develop allergens than children who switch to producing Th1
83
take a minute to breath
a whole minute!!!
84
Tell me about the management of IgE mediated allergic disorders
Avoidance of allergen Block mast cell allergen - medication Prevent effects of mast cell activation - anti-histamines Anti-inflammatory agents - removes Th2 cells Adrenaline - epi-pen
85
What is type II hypersensitivity reactions (direct cell effects) mediated by
IgM/IgG antibodies bind to antigens present on cell surfaces or ECM. this marks the cell for destruction
86
Type IIa reactions
destruction of antigen-positive cells
87
Type IIb reactions
stimulation of cell surface antigens
88
Tell me the summary table (because you lazy) of the 4 types of hypersensitivity reactions
Type 1 - antibody mediated immunity, IgE, Fast response (minutes), allergic reactions, asthma/allergic rhinitis Type 2 - antibody mediated immunity, IgG/IgM, Intermediate, body cells directly attacked by antibodies, Rheumatic heart disease Type 3 - antibody mediated immunity, IgG/IgM, intermediate, complex accumulation and destruction, rheumatoid arthritis Type 4 - cell mediated immunity, Th1, late response (48-72 hours), cell mediated cytotoxicity, transplant rejection/contact dermatits
89
Tell me about resolution
normal immune response pathogen cleared tissure repair
90
Tell me about the response to a latent infection
normal immune response pathogen controlled infection can re-occur
91
Tell me about the response to chronic infection
Defective immune response Pathogen not cleared or controlled
92
What are primary immunodeficiencies a result of
genetic defects
93
What are secondary immunodeficiencies caused by
environmental factors, such as HIV or malnutrition
94
What does SPUR stand for - PRIMARY IMMUNE DEFICIENCY
Serious infections, persistent infections, unusual infections, recurrent infections
95
Are serious infections responsive or unresponsive to oral antibiotics
unresponsive
96
What are other features that suggest primary immune deficiency
Weight loss severe skin rash chronic diarrhoea cancer family history