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REVISION > chronic adaptive repair > Flashcards

chronic adaptive repair Flashcards

1
Q

what type of inflammation would occur as a result of persistent bouts of acute inflammation? with example.

A

non specific
periodontitis

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2
Q

what’s the infiltrate dominated by in non specific chronic inflammation?

A

tissue macrophages
B cells
t cells

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3
Q

what are the 5 stages of periodontitis?

A

initiation
progression
amplification
resolution (acute) or no resolution (chronic)

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4
Q

what can induce specific primary chronic inflammation?

A

arises de novo and perisistant exposure

non immunological agents eg noxious materials, foreign body reactions
or
immunological agents eg infectious organisms, hypersensitivity, autoimmune, infections

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5
Q

what characterises specific primary chronic inflammation?

A

excessively activated macrophages

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6
Q

give an example of a specific chronic inflammation?

A

autoimmune diseases like rheumatoid arthritis

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7
Q

what is an autoimmune disease? and cause

A

unwanted response of body own cells and tissues
- loss of tolerance to self antigens or commensal bacteria

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8
Q

what are the tolerance mechanisms to prevent autoimmunity?

A

positive and negative selection

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9
Q

what happens in rheumatoid arthritis?

A

auto reactive T cells against antigens of joint synovium

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10
Q

how does periodontal disease link to rheumatoid arthritis ?

A

produces PAD enzymes which citrillunate Argentine to citrulline
which leads to loss of tolerance (b and T cells attach citrilunine proteins)

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11
Q

how does chronic granulomatous inflammation differ from normal chronic inflammation?

A

contain modified activated macrophages (epitheliod macrophages)

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12
Q

how do modified activated macrophages differ from normal ones?

A

less phagocytic more secretory so produce more cytokines and chemokines

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13
Q

what are giant cells?

A

fused epitheliod macrophages

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14
Q

what causes chronic granulomatous inflammation?

A

immunological eg invading pathogens and delayed hypersensitivity
or
non immunological eg foreign body in tissue such as asbestos

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15
Q

what do granulomas do?

A

form around pathogens and foreign material that the immune system can’t remove
- prevent them from spreading round body

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16
Q

what macrophages are involved in tissue injury?

A

m1 pro inflammatory

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17
Q

what macrophages are involved in tissue repair?

A

m2 anti-inflammatory

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18
Q

what do m1 macrophages produce?

A

proteases
neutrophil chemotactic factors
nitric oxide
coagulation factors

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19
Q

what do m2 macrophages produce?

A

fibrosis
growth factors
angiogenesis
fibrogenic cytokines

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20
Q

how does a granuloma form?

A

macrophages present antigen to lymphocytes
- lymphocytes produce cytokines
- epithelia macrophages form
- giant cell forms
- giant cells engulf foreign material
back to start

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21
Q

give example of chronic granulomatosis formation?

A

ororfacial granulomatosis

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22
Q

what happens in chronic periodontitis?

A

destruction of soft and hard tissues

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23
Q

what is the stages of periodontitis?

A
  1. initiation of immune response
  2. immune cell recruitment
  3. immune cell activated
  4. RANKL produces
  5. osteoclasts activated
  6. reduced function of osteoblasts
  7. MMPs activated
    not 456 hard tissue
    7 soft tissue
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24
Q

what produces MMPs?

A

immune cells produce different types

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25
Q

what is the function of matrix metalloproteinases?

A

soft tissue destruction
remodel the ECM that supports cells
- angiogenesis
- cell migration

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26
Q

how often do we get a new skeleton and why?

A

10 years as bone constantly remodelled

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27
Q

what happens in periodontitis for alveolar bone destruction?

A

more osteoclastogenesis
RANKL activates osteoclasts
therefor more bone resorption

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28
Q

where do osteoclasts differentiate from?

A

macrophages

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29
Q

in health how is osteoclastogenesis controlled?

A

RANKL production controlled by OPG so no bone resorption

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30
Q

what produces RANKL and OPG?

A

osteoblasts

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31
Q

where is the RANKL receptor?

A

osteoclasts to control bone resorption

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32
Q

what is OPG and how does it work?

A

osteoprogerin
inhibits RANKL from binding to RANK receptor

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33
Q

what does RANKL mean?

A

receptor activator of nuclear Kappa b ligand

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34
Q

what is bone remodelling a balance between?

A

RANKL/OPG ratio

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35
Q

how do we stimulate osteoblasts to produce more RANKL in periodontitis?

A
  • p gingivalis recognised by osteoblasts via receptor recognition
  • downstream signalling cascade
  • RANKL produced
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36
Q

what is adaptive immunity?

A

cell mediated and humoral responses

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37
Q

what do T cells do?

A

drive cell mediated immunity

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38
Q

what do B cells do?

A

drive humoral immunity and produce antibodiess

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39
Q

what is immunological memory?

A

pathogen remember by b or T cell receptor incase it invades again

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40
Q

how long does the adaptive immune response take to be activated?

A

after 4 to 7 days

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41
Q

when would adaptive immunity kick in?

A

if the infection can’t be controlled by innate immune system

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42
Q

why do we feel unwell with an infection?

A

as adaptive immune response takes a while to kick in

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43
Q

what are the 3 main receptors in adaptive immunity?

A

T cell receptor
B cell receptor
major histocompatibility complex (MHC proteins)

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44
Q

what is the difference between innate and adaptive receptors?

A

adaptive receptors can change shape to recognise different antigens

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45
Q

where are T cells derived from and where do they mature?

A

bone marrow and mature in thymus

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46
Q

what do T cells give rise to?

A

cellular immunity

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47
Q

what to TCRs recognise?

A

antigens presented by antigen presenting cells

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48
Q

what is T cell repertoire?

A

T cells can respond to numerous different antigens (diversity in receptor )

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49
Q

what is in place to ensure T cells dont respond to self peptides?

A

thymus education

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50
Q

what is the function of t helper cells? CD4+

A

support other immune cells fight threat

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51
Q

what is the function of cytotoxic T cells? CD8+

A

destroy your own cells which have become infected

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52
Q

what do regulatory T cells do? (tregs)

A

regulate or suppress other cells in immune system

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53
Q

what do all T cells start as?

A

nieve T cells with receptor for specific antigen

54
Q

what does CD8 cor receptor bind do?

A

MHC I

55
Q

what does CD4 coreceptor bind to?

A

MHC II

56
Q

what does CD3 coreceptor do?

A

activated CD4+ and CD8+

57
Q

what cells express MHC I?

A

infected host cells

58
Q

what cells express MHC II?

A

APC

59
Q

what is a marker for identifying T cells?

A

CD3

60
Q

what protein chains make up majority of T cell receptors?

A

alpha and beta chains

61
Q

what protein chains make up 5 % of T cell receptors ?

A

gamma and delta chains

62
Q

what are the 2 parts of alpha and beta chains on t cell receptors?

A

constant = bottom
variable = antigen binding site

63
Q

what codes for the variable region on a T cell receptor?

A

variable = a and b
diversity = b only
joining = a and b

64
Q

how are genes rearranged on a T cell receptor? what does it lead to?

A

somatic recombination by RAG enzymes
different receptors to recognise different antigens

65
Q

what happens to T cells in the thymus?

A

interact with thymic cortical epithelial cells
- positive and negative selection

66
Q

what is positive selection in the thymus?

A

no recognition leads to apoptosis

67
Q

what is negative selection in the thymus?

A

recognise self antigen leads to apoptosis

68
Q

how does T cells survive positive and negative selection in the thymus?

A

moderate binding postitive selection

69
Q

after thymic education where do some T cells reside?

A

lymph nodes

70
Q

when do T cells change from nieve T cells?

A

when they interact with antigen

71
Q

where do dendritic cells take up and process the antigen?

A

epidermis

72
Q

once dendritic cells have taken up the antigen what do they do?

A

migrate to the lymph nodes and mature on the way

73
Q

what primes nieve T cells?

A

dendritic cells

74
Q

what is required to activate a T cell?

A

3 signals
1. activation of T cell
2. survival and clonal expansion
3. differentiated into subsets (4) or effector function (8)

75
Q

what happens if nieve t cells have signal 1 but not signal 2?

A

anergy - don’t function as they should

76
Q

what happens if nieve T cells signal 1 and 2 but not 3?

A

apoptosis

77
Q

what is the role of T helper 1 cells?

A

support/ activate macrophage via interferon gamma

78
Q

what is the function of t helper 2 cells?

A

source of IL- 4 5 6 cytokines which tell B cell to produce antibodies

79
Q

what is the function of t helper 17 cells?

A

kill extracellular bacteria by producing IL17 cytokine - tell epithelium what to do

80
Q

where are t follicular helper cells found ? what do they do?

A

B cell zone in secondary lymphoid organs
- tell B cells to produce antibody

81
Q

what is function of tregs?

A

immune suppression
release IL10 to inhibit T cell and DC activation

82
Q

how does a CD8+ T cell arise?

A

interaction between MHC 1 and TCR

83
Q

how does a CD4+ cell arise?

A

interaction between MHC 2 and TCR

84
Q

what is the function of CD8+ T cells?

A

induce apoptosis by producing granzyme and perforin

85
Q

what are plasma cells?

A

antibody factories

86
Q

what are memory B cells?

A

allow for a quicker response to subsequent infections when they returns

87
Q

how do B cells recognise antigens?

A

B cell receptor (which is antibody IgM or IgD)

88
Q

what is another name for B cell receptor?

A

immunoglobulins Ig

89
Q

what are the 5 antibody immunoglobulins?

A

IgM and IgD B cell receptor
IgG and IgM and IgA produced and released by B cell

90
Q

what is the most common antibody? 80%
what are they resistant against?

A

IgG
viruses and bacteria

91
Q

what does IgE attach to and why?

A

basophils and mast cells to degranulate for allergic reaction

92
Q

what other antibody has role in allergy?

A

IgD

93
Q

what is the first class of antibodies produced after antigen is encountered? how many binding sites?

A

IgM
10 = pentamer

94
Q

where is IgA found?

A

glandular secretions to attack pathogens

95
Q

how do BCR structure differ from TCR?

A

BCR has light and heavy chains in constant region and variable

96
Q

what happens in each development stage of B cells?
where does this happen?
what happens next?

A

rearranging of Ig heavy and light chains
in bone marrow then enters periphery and migrate to secondary lymphoid organs

97
Q

what regions are involved in heavy and light chains in B cell receptor diversity?

A

heavy = V D J
light = V J

98
Q

what is immature B cell receptor mainly made up of? what is mature?

A

IgM
IgM and IgD

99
Q

what must B cells do before leaving bone marrow?

A

go through negative selection

100
Q

what does negative selection of B cells prevent?

A

they dont react with self antigens

101
Q

what removes self reacting B cells?

A

macrophages

102
Q

what happens if B cell reacts with self antigen during negative selection?

A

retained in bone marrow

103
Q

what happens if there’s no reaction of B cell with self antigen in negative selection?

A

moves to blood and expresses IgD and IgM

104
Q

what are the 3 main functions of antibodies produced by B cells?

A
  • neutralisation
  • opsonisation = coating of pathogen by antibody
  • complement initiation = classical
105
Q

what is primary goal of antibodies produced by B cells?

A

prevent microbial activity and aid removal of threat from host
- promotes phagocytosis

106
Q

what are 2 ways a B cell can become activated?

A

thymus dependant antigens = require T cell help
thymus independant antigens

107
Q

where does B cell activation occur?

A

lymph nodes

108
Q

what does the activation of B cells result in?

A

plasma cells
or
memory B cells

109
Q

what is produced in T cell independent activation?

A

plasma cells

110
Q

what is produced in T cell dependent B cell activation?

A

plasma cells
memory B cells

111
Q

what is a disadvantage of T cell independent B cell activation?

A

doesn’t lead to memory B cells so no long term immunity
- due to the response being weaker

112
Q

what leads to class switching?

A

activation of B cell

113
Q

why do we do class switching?

A

as IgM response week so class switch to IgG for an increased affinity for antibody

114
Q

what is affinity in antibody?

A

strength of binding of single antibody to antigen

115
Q

what is avidity in antibody?

A

ability of antibodies to form complexes

116
Q

what is avidity in antibody?

A

ability of antibodies to form complexes

(no of binding sites)

117
Q

what is the difference between affinity and avidity of IgM and IgG?

A

IgM has decreased affinity and increased avidity
therefor IgG better

118
Q

why would B cells class switch from IgM to IgE?

A

allergy

119
Q

where do b and T cell interactions occur?

A

germinal centres

120
Q

what is the basic principle of vaccination?

A

IgM produced from B cells = 4 days
IgM to IgG = 1 and 1/2 week
- on second exposure IgG for readily produced right away!

121
Q

what is tolerance important in?

A

immune unresponsiveness

122
Q

what are the 2 types of tolerance?

A

central = primary lymphoid organs
peripheral = out with thymus and bone marrow

123
Q

what is central tolerance in T cells?

A

positive and negative selection in thymus

124
Q

what is central tolerance for B cells?

A

negative selection in the bone marrow

125
Q

what is central tolerance for B cells?

A

negative selection in the bone marrow

126
Q

is tolerance mechanism is dysfunctional what would happen (breach of tolerance)?

A

autoimmune disease

127
Q

what does peripheral tolerance do?

A

prevents the activation of self reactive T cells that were not eliminated

128
Q

what are the 3 ways peripheral tolerance stops activation of self reactive T cells?

A

anergy
apoptosis
t regulatory cells

129
Q

why do most self reactive B cells become anergic?

A

as they require help from self reactive T cells but majority are eliminated during tolerance

130
Q

what do central and peripheral tolerance mechanisms prevent?

A

autoimmunity

REVISION (12 decks)

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