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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
what is the function of matrix metalloproteinases?
soft tissue destruction remodel the ECM that supports cells - angiogenesis - cell migration
26
how often do we get a new skeleton and why?
10 years as bone constantly remodelled
27
what happens in periodontitis for alveolar bone destruction?
more osteoclastogenesis RANKL activates osteoclasts therefor more bone resorption
28
where do osteoclasts differentiate from?
macrophages
29
in health how is osteoclastogenesis controlled?
RANKL production controlled by OPG so no bone resorption
30
what produces RANKL and OPG?
osteoblasts
31
where is the RANKL receptor?
osteoclasts to control bone resorption
32
what is OPG and how does it work?
osteoprogerin inhibits RANKL from binding to RANK receptor
33
what does RANKL mean?
receptor activator of nuclear Kappa b ligand
34
what is bone remodelling a balance between?
RANKL/OPG ratio
35
how do we stimulate osteoblasts to produce more RANKL in periodontitis?
- p gingivalis recognised by osteoblasts via receptor recognition - downstream signalling cascade - RANKL produced
36
what is adaptive immunity?
cell mediated and humoral responses
37
what do T cells do?
drive cell mediated immunity
38
what do B cells do?
drive humoral immunity and produce antibodiess
39
what is immunological memory?
pathogen remember by b or T cell receptor incase it invades again
40
how long does the adaptive immune response take to be activated?
after 4 to 7 days
41
when would adaptive immunity kick in?
if the infection can't be controlled by innate immune system
42
why do we feel unwell with an infection?
as adaptive immune response takes a while to kick in
43
what are the 3 main receptors in adaptive immunity?
T cell receptor B cell receptor major histocompatibility complex (MHC proteins)
44
what is the difference between innate and adaptive receptors?
adaptive receptors can change shape to recognise different antigens
45
where are T cells derived from and where do they mature?
bone marrow and mature in thymus
46
what do T cells give rise to?
cellular immunity
47
what to TCRs recognise?
antigens presented by antigen presenting cells
48
what is T cell repertoire?
T cells can respond to numerous different antigens (diversity in receptor )
49
what is in place to ensure T cells dont respond to self peptides?
thymus education
50
what is the function of t helper cells? CD4+
support other immune cells fight threat
51
what is the function of cytotoxic T cells? CD8+
destroy your own cells which have become infected
52
what do regulatory T cells do? (tregs)
regulate or suppress other cells in immune system
53
what do all T cells start as?
nieve T cells with receptor for specific antigen
54
what does CD8 cor receptor bind do?
MHC I
55
what does CD4 coreceptor bind to?
MHC II
56
what does CD3 coreceptor do?
activated CD4+ and CD8+
57
what cells express MHC I?
infected host cells
58
what cells express MHC II?
APC
59
what is a marker for identifying T cells?
CD3
60
what protein chains make up majority of T cell receptors?
alpha and beta chains
61
what protein chains make up 5 % of T cell receptors ?
gamma and delta chains
62
what are the 2 parts of alpha and beta chains on t cell receptors?
constant = bottom variable = antigen binding site
63
what codes for the variable region on a T cell receptor?
variable = a and b diversity = b only joining = a and b
64
how are genes rearranged on a T cell receptor? what does it lead to?
somatic recombination by RAG enzymes different receptors to recognise different antigens
65
what happens to T cells in the thymus?
interact with thymic cortical epithelial cells - positive and negative selection
66
what is positive selection in the thymus?
no recognition leads to apoptosis
67
what is negative selection in the thymus?
recognise self antigen leads to apoptosis
68
how does T cells survive positive and negative selection in the thymus?
moderate binding postitive selection
69
after thymic education where do some T cells reside?
lymph nodes
70
when do T cells change from nieve T cells?
when they interact with antigen
71
where do dendritic cells take up and process the antigen?
epidermis
72
once dendritic cells have taken up the antigen what do they do?
migrate to the lymph nodes and mature on the way
73
what primes nieve T cells?
dendritic cells
74
what is required to activate a T cell?
3 signals 1. activation of T cell 2. survival and clonal expansion 3. differentiated into subsets (4) or effector function (8)
75
what happens if nieve t cells have signal 1 but not signal 2?
anergy - don't function as they should
76
what happens if nieve T cells signal 1 and 2 but not 3?
apoptosis
77
what is the role of T helper 1 cells?
support/ activate macrophage via interferon gamma
78
what is the function of t helper 2 cells?
source of IL- 4 5 6 cytokines which tell B cell to produce antibodies
79
what is the function of t helper 17 cells?
kill extracellular bacteria by producing IL17 cytokine - tell epithelium what to do
80
where are t follicular helper cells found ? what do they do?
B cell zone in secondary lymphoid organs - tell B cells to produce antibody
81
what is function of tregs?
immune suppression release IL10 to inhibit T cell and DC activation
82
how does a CD8+ T cell arise?
interaction between MHC 1 and TCR
83
how does a CD4+ cell arise?
interaction between MHC 2 and TCR
84
what is the function of CD8+ T cells?
induce apoptosis by producing granzyme and perforin
85
what are plasma cells?
antibody factories
86
what are memory B cells?
allow for a quicker response to subsequent infections when they returns
87
how do B cells recognise antigens?
B cell receptor (which is antibody IgM or IgD)
88
what is another name for B cell receptor?
immunoglobulins Ig
89
what are the 5 antibody immunoglobulins?
IgM and IgD B cell receptor IgG and IgM and IgA produced and released by B cell
90
what is the most common antibody? 80% what are they resistant against?
IgG viruses and bacteria
91
what does IgE attach to and why?
basophils and mast cells to degranulate for allergic reaction
92
what other antibody has role in allergy?
IgD
93
what is the first class of antibodies produced after antigen is encountered? how many binding sites?
IgM 10 = pentamer
94
where is IgA found?
glandular secretions to attack pathogens
95
how do BCR structure differ from TCR?
BCR has light and heavy chains in constant region and variable
96
what happens in each development stage of B cells? where does this happen? what happens next?
rearranging of Ig heavy and light chains in bone marrow then enters periphery and migrate to secondary lymphoid organs
97
what regions are involved in heavy and light chains in B cell receptor diversity?
heavy = V D J light = V J
98
what is immature B cell receptor mainly made up of? what is mature?
IgM IgM and IgD
99
what must B cells do before leaving bone marrow?
go through negative selection
100
what does negative selection of B cells prevent?
they dont react with self antigens
101
what removes self reacting B cells?
macrophages
102
what happens if B cell reacts with self antigen during negative selection?
retained in bone marrow
103
what happens if there's no reaction of B cell with self antigen in negative selection?
moves to blood and expresses IgD and IgM
104
what are the 3 main functions of antibodies produced by B cells?
- neutralisation - opsonisation = coating of pathogen by antibody - complement initiation = classical
105
what is primary goal of antibodies produced by B cells?
prevent microbial activity and aid removal of threat from host - promotes phagocytosis
106
what are 2 ways a B cell can become activated?
thymus dependant antigens = require T cell help thymus independant antigens
107
where does B cell activation occur?
lymph nodes
108
what does the activation of B cells result in?
plasma cells or memory B cells
109
what is produced in T cell independent activation?
plasma cells
110
what is produced in T cell dependent B cell activation?
plasma cells memory B cells
111
what is a disadvantage of T cell independent B cell activation?
doesn't lead to memory B cells so no long term immunity - due to the response being weaker
112
what leads to class switching?
activation of B cell
113
why do we do class switching?
as IgM response week so class switch to IgG for an increased affinity for antibody
114
what is affinity in antibody?
strength of binding of single antibody to antigen
115
what is avidity in antibody?
ability of antibodies to form complexes
116
what is avidity in antibody?
ability of antibodies to form complexes (no of binding sites)
117
what is the difference between affinity and avidity of IgM and IgG?
IgM has decreased affinity and increased avidity therefor IgG better
118
why would B cells class switch from IgM to IgE?
allergy
119
where do b and T cell interactions occur?
germinal centres
120
what is the basic principle of vaccination?
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
what is tolerance important in?
immune unresponsiveness
122
what are the 2 types of tolerance?
central = primary lymphoid organs peripheral = out with thymus and bone marrow
123
what is central tolerance in T cells?
positive and negative selection in thymus
124
what is central tolerance for B cells?
negative selection in the bone marrow
125
what is central tolerance for B cells?
negative selection in the bone marrow
126
is tolerance mechanism is dysfunctional what would happen (breach of tolerance)?
autoimmune disease
127
what does peripheral tolerance do?
prevents the activation of self reactive T cells that were not eliminated
128
what are the 3 ways peripheral tolerance stops activation of self reactive T cells?
anergy apoptosis t regulatory cells
129
why do most self reactive B cells become anergic?
as they require help from self reactive T cells but majority are eliminated during tolerance
130
what do central and peripheral tolerance mechanisms prevent?
autoimmunity

REVISION (12 decks)

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