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CMB1003- Microbiology and immunology > immunity L18-26 > Flashcards

immunity L18-26 Flashcards

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1
Q

immunity

A

the ability of an organism to resist a particular infection by a pathogen by the action of specialized cells o molecules

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2
Q

2 types of natural immunity

A

innate
acquired/ adaptive

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3
Q

innate immunity

A

present at birth
cells patrol for infection
simple recog systems that identify common pathogen structures
rapid response
many cell types
limited capacity

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4
Q

acquired immunity

A

specific pathogen recog
not present at birth
learnt from invading organisms
slower response
highly specialised cells
generate “memory”

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5
Q

immune system goal

A

to clear/kill; potential pathogens in a controlled/ efficient process
- limited pathology to host
- return to homeostasis
- confer future protection against same pathogen
- check for non-healthy cells

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6
Q

factors affecting immunity

A

general health
infection
nutrition
environmental conditions
microbiome
pregnancy
genetics
stress

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7
Q

Edward Jenner

A

small pox immunity
18th century

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8
Q

Louis Pasteur

A

cholera vaccination w attenuated organisms

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9
Q

vaccines

A

substance used to stimulate production of immunity against 1/ several diseases without inducing disease
made up of: disease causative agent/ products/ synthetic substitute

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10
Q

measles and herd immunity

A

need > 95% immune population to prevent measles outbreak
MMMR vaccine in 1988
Andrew Wakefield false link between MMR and autism

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11
Q

why no vaccines for malaria/ HIV/ ebola

A

complex pathogens
pathogen life cycle understanding
expensive/ time consuming clinical trials

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12
Q

4 main groups of vaccines

A

live
killed (attenuated/ inactivated)
subunits
nucleic acid

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13
Q

innate responses

A

humoral (molecules found in fluids)
cellular (found in blood as well as tissues)

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14
Q

antibodies

A

soluble glycoproteins secreted by B-lymphocytes

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15
Q

serology

A

identifying/ measuring antibodies present in blood
- useful for measuring pathogen response

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16
Q

clonal selection

A

B and T cells expanded populations of individual clones expressing unique Ag receptor

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17
Q

how do cells of immune system circulate?

A

via blood and lymphatics

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18
Q

primary/ central lymphoid tissues

A

bone marrow
thymus

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19
Q

bone marrow

A

soft spongy, cellular tissue filling internal cavity of bones
- B/T cells continuous generation

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20
Q

thymus

A

specialized/ v cellular gland
- T cells educated here > only 2-4% survive and exit

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21
Q

mature lymphocytes

A

clonally diverse
each B and T cell have single antigen receptor
Ag specific

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22
Q

secondary/ peripheral lymphoid tissues

A

B and T lymphocytes recirculate via blood/ lymphatics through tissues until antigen meet and undergo clonal expansion/ differentiation in tissues

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23
Q

effector mechanisms factors for immune response

A

pathogen type
location

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24
Q

innate defence mechanisms

A

barriers
cellular defences
molecular defences (humoral factors)

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25
Q

physical and chemical barriers to infection

A

skin (physical barrier/ fatty acids/ commensals)
mucus membranes (mucus/ cilia/ commensals/ low pH)
lysozyme in tears
stomach acid

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26
Q

antibacterial enzymes in body

A

lysozyme
secretory phospholipase A2
tears/ saliva/ phagocytes

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27
Q

AMP

A

antimicrobial peptides

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28
Q

need for recognition in the immune system

A

discriminate between self/ non-self
multiple pathogen defence
immunity component deficiencies

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29
Q

PRR

A

pattern recognition receptors

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30
Q

PRR locations

A

host cells>
macrophages
neutrophils
dendritic cells

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31
Q

PRR functions

A

allow pathogen identification
recognise simple molecules/ patterns
‘lock and key mechanism’

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32
Q

types of PRR

A

toll-like receptors
NOD-like receptors
RIG-I-like helicases

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33
Q

toll-like receptors

A

repertoire of pathogen-associated molecular patterns (PAMPs)
*10 in humans

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34
Q

NOD-like receptors

A

nucleotide-binding oligomerisation domain

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35
Q

PAMPs

A

mannose-rich oligosaccharides
peptidoglycans
lipopolysaccharides
unmethylated CpG DNA

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36
Q

leucocyte production

A

pluripotent haematopoietic stem cells in bone marrow

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37
Q

leucocyte cells

A

lymphocytes
monocytes
granulocytes
neutrophils
eosinophils
basophils
tissue mast cells

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38
Q

macrophage activated function

A

phagocytosis/ bactericidal mechanisms
antigen presentation

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39
Q

dendritic cell activated function

A

antigen uptake in peripheral sites
antigen presentation

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40
Q

neutrophil activated function

A

phagocytosis
activation of bactericidal mechanisms

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41
Q

eosinophil activated function

A

killing of antibody-coated parasites

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42
Q

basophil activated function

A

promotion of allergic responses
augmentation of anti-parasitic immunity

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43
Q

mast cell activated function

A

release of granules containing histamine and active agents

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44
Q

location of dendritic cells

A

around lymphatic system
big sa
specialised antigen presenting

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45
Q

innate immunity cells

A

granulocytes>
neutrophils/ eosinophils/ basophils/ monocytes

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46
Q

adaptive immunity cells

A

B cell
T cell

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47
Q

cellular defences

A

phagocytosis
extracellular killing
inflammation

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48
Q

phagocyte pathologies

A

bacterial infections
fungal infections
recurrent infections
e.g. leukocyte adhesion disease syndromes > unable to make pus

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49
Q

phagocytosis

A

ingestion and killing of microorganisms by specialised cells

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50
Q

neutrophils

A

short-lived (<24h)
multi-lobed nucleusabundant in sites of acute inflammation
most common

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51
Q

PMN

A

polymorphonuclear cells

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52
Q

mononuclear phagocytes

A

blood monocytes
macrophage in tissue
longer lived (months)

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53
Q

phagocytosis process

A
  1. RECOG macrophage expresses receptors for bacterial constituents (components/ complement/ antibody)
    bacteria binding to macrophage receptors initiate cytokine release
  2. INTERNALISATION in membrane-bound vacuole engulfment and digestion
  3. RELEASE
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54
Q

phagolysosome

A

phagasome fusion with lysosome

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55
Q

phagocytic killing mechanisms

A

acidification
toxic nitrogen oxides
antimicrobial peptides
enzymes
competitors

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56
Q

oxygen-dependent killing

A

hexose monophosphate shunt > NADPH generation
NADPH oxidase generates reactive oxygen intermediates
CGD problem w NADPH pathway

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57
Q

reactive oxygen intermediates characteristics

A

bacteriostatic/ bactericidal

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58
Q

macrophages additional functions

A

activated by bacterial products/ cytokines
secrete cytokines
present antigen to lymphocytes

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59
Q

extracellular killing

A

active against organisms too large for phagocytosis/ infected cells

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60
Q

cells involved in extracellular killing

A

eosinophils
natural killer T cells

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61
Q

natural killer T cells

A

innate cells lacking antigen-specific receptors
active against viral infected cells
attack some tumour cells
release lytic granules (granzyme/ perforin)

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62
Q

NK cells

A

activated by cytokines
can produce IFN > control infections
contain viral infections whilst adaptive/ specific response kicks in

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63
Q

NK cell deficiency

A

increased herpes risk

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64
Q

cytokines

A

innate and adaptive
low molecular weight proteins (5-25kDa) secreted by cells stimulating/ inhibiting activity/ proliferation/ differentiations of other cells
20
sub-groups of interferons, lymphokines, interleukins, chemokines

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65
Q

complement

A

protection in early infections
affector system of humoral branch of innate / adaptive immune response
group of nearly 30 serum and membrane proteins
initial activation and regulated enzyme cascade

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66
Q

complement goal

A

inflammation / phagocytosis / membrane attack for pathogen kill

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67
Q

complement roles

A

opsonizing of bacteria
regulate inflammatory response
activate B cells
membrane attack complex for pathogen lysis

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68
Q

3 pathways of complement activation

A

classical pathway
lectin pathway
alternative pathway

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69
Q

classical complement pathway

A

antibody binds to specific antigen on pathogen surface

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70
Q

lectin complement pathway

A

mannose-binding protein binds to pathogen surface
acute phase protein initiation binding glycoproteins/ carbs on micro-organisms

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71
Q

alternative complement pathway

A

pathogen surface creates local environment conducive to complement activation

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72
Q

complement activation effects

A

recruitment of inflammatory cells
opsonization of pathogens, facilitating uptake and killing by phagocytic cells
lysis and death of pathogens
C3 CONVERTASE GENERATION > membrane attack complex production

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73
Q

nomenclature of classical pathway

A

C(number)
cleavage reaction products designated w different uppercase letters

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74
Q

alternative pathway nomenclature

A

factor D
factor B
properdin (factor P)

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75
Q

classical pathway structure

A

C1 (complement activation first component) = C1q/ C1r/ C1s complex
2 molecules of C1r/C1s bind to each C1q

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76
Q

classical pathway process

A

pentameric IgM binds to antigens (‘staple form’)
C1q binds to IgG molecules > activates C1r> cleaves and activates serine protease C1s

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77
Q

C1q molecule

A

6 globular heads joined to common stem
each head can bind to one Fc domain on an antibody
>2 globular heads bind to Fc domains for C1q activation

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78
Q

C1q binding

A

to single IgM/ 2+ IgG > conformational change > proteoytic site reveal on C1r

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79
Q

C1r

A

enzymatic activity when proteolytic site revealed
cleaves C1s > serine protease enzyme C1s

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80
Q

C1s

A

active
cleaves C4 > C4a/C4b
cleaves C2 after binding to C4b > C4b2a complex (C3 convertase)

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81
Q

C3 convertase

A

c4b2a complex
cleaves C3 molecules > C3b/ C3a
therefore many C3b on pathogen surface

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82
Q

effect of many C3b on pathogen surface

A

opsonisation of pathogens
phagocytosis of pathogen by cells w complement receptors
can also activate alternative pathway > further amplification

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83
Q

c3b if doesn’t bind to pathogen surface immediately

A

rapid hydrolysis by water
inactive

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84
Q

MAC overview

A

C4b2a3b + C5
C5 cleaved > C5a/C5b
C5b + C6 > C5bC6
C5bC6 +C7 > C5b67
conformational change and C7 insertion into lipid bilayer
C8 +Cb5b67 +C9 and polymerise
membrane pore formation

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85
Q

MAC

A

membrane attack complex
- displaces cell membrane phospholipids
- channel
membrane disruption
cell lysis
death

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86
Q

alternative pathway

A

can be activated by lectin/ classical pathway/ C3 spontaneous hydrolysis
C3b binding to factor B
factor D cleaves into Ba/Bb
C3bBb C3 convertase
properdin stabilizes

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87
Q

alternative pathway process

A

C5b binds C6/C7
C5b67 complexes bind to membrane via C7
C8 binds and inserts into membrane
10-16 C9 molecules form membrane pore

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88
Q

lectin pathway

A

soluble receptors
recognise microbial surface/ activate complement cascade
CHO on microbial surface
mannose complexes binding lectin and MBL-associated serine proteases
MASP-1/MASP-2 (cleaves C4/C2)
cleavage and activation

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89
Q

lectin pathway process

A

activated MASP-2 w MBL/ Ficolin l cleaves C4 > C4a and C4b
C4b binds C2 / MASP-2 cleaved >C2a/C2b and C4b2a complex
many c3b molecules on surface

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90
Q

lectin pathway comparison to classical

A

same C3 convertase
same C5 convertase
initiated differently

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91
Q

C3 deficiency

A

life-threatening infections w bacterial range
opsonisation/ inflammation/ cytolysis functions affected

92
Q

C6/C7/C8/C9 deficiency

A

cytolysis affected
neisseria infection problems

93
Q

cytokine secretion

A

by immune cells
brief-self-limited event
pleitropic/ redundant

94
Q

pleotropic

A

multiple biological actions

95
Q

redundant

A

shared biological actions

96
Q

cytokine action initiation

A

bind to specific membrane receptors on target cells

97
Q

cytokine regulation

A

via external signals regulating cytokine receptors/ responsiveness of cells to them

98
Q

cellular response to most cytokines

A

changes in gene expression of target cells
expression of new functions
proliferation of target cells

99
Q

3 major functional categories of cytokines

A
  1. mediators/ innate immunity regulators
  2. mediators/ adaptive immunity regulators
  3. haematopoiesis stimulators
100
Q

mediators and regulators of innate immunity

A

produced by macrophages in response to infection

101
Q

ediators and regulators of adaptive immunity

A

produced by T lymphocytes in response to antigen recognition

102
Q

haematopoiesis stimulators

A

bone marrow stromal cell/ leukocyte production
stimulate growth/ differentiation of immature leukocytes

103
Q

important cytokines

A

IL2
IL1
TNFa
interferons

104
Q

chemokines

A

chemotractive cytokines
CXC/CC group

105
Q

effects of cytokines secreted by macrophages

A

inflammation (chemotactic/ act on vascular endothelium)
fever
acute phase response
act on lymphocytes

106
Q

antimicrobial mechanisms of phagocytes

A

acidification
toxic oxygen-derived products
toxic nitrogen oxides
antimicrobial peptides
enzymes
competitors

107
Q

antimicrobial peptides

A

innate
ampipathic> lipid bilayer> destabilis
immunomodulatory effects on host cells

108
Q

signs of inflammation

A

oedema
erythema
heat
pain
loss of function

109
Q

inflammation mechanisms

A

brings cells and molecules from blood to site
^blood supply via vasodilation
^ adhesion molecule expression

110
Q

inflammation aim

A

restore homeostasis
limit damage
recovery

111
Q

inflammation triggers

A

pathogens
tissue damage
disruptive/ inappropriate immune response

112
Q

inflammation process

A

bacteria trigger macrophage to release cytokines/ chemokines
vasodilation / ^vascular permeability cause redness, swelling and heat
inflam cells migrate into tissue> release inflam mediators

113
Q

inflammation mediators

A

complement products
macrophage/ t-cell-derived cytokines
mast cells

114
Q

local inflammation

A

PRR on macrophage stimulated
TNFa release
positive outcome

115
Q

endotoxic shock

A

excessive cytokine release in gram-negative bacterial infection
vascular endothelium effects> circulatory shock / DIC

116
Q

DIC

A

disseminated intravascular coagulation

117
Q

toxic shock/ systemic inflammation

A

PRR on macrophage stimulated
TNFa release uncontrolled
negative outcome

118
Q

cytokine storm

A

^circulating cytokines level
immune cell hyper-activation
immune response> organ failure/ DIC

119
Q

GI host-immune interactions

A

tight junctions
paneth cells secrete AMPs/ IgA secretion
complement
saliva/pH/bile/peristalsis
microbiome

120
Q

microbiome host immune interaction

A

supresses proliferation/ colonization of pathogens
IL1 beta activation/ AMP production/ TH17 cell differentiation

121
Q

Crohn’s disease

A

inflam bowel disease
autoimmune
autoreactive T cells against intestinal floral antigens

122
Q

Crohns treatment

A

immunomodulation
surgery
diet

123
Q

antibodies

A

immunoglobulins Ig
‘y-shaped’ secreted glycoproteins
bind to specific Ags

124
Q

hat do antibodies bind to

A

proteins/ polysaccharides/ lipids/ nucleic acids/ chemicals/ metals

125
Q

Ig basic units

A

2 identical heavy chains + 2 identical light chains
non-covalent interaction/ disulphide bridge connections
N-terminal variable region on each chain

126
Q

Ig secretion and expression

A

secreted from mature B-cells
expressed as membrane-bound B cell antigen receptor

127
Q

Fab

A

fragment antigen binding fragment
contains antigen-binding region
bind to epitopes on pathogens
allows antibody and Ags w high affinities

128
Q

Fc

A

fragment crystalizable fragment

129
Q

antibodies funcions

A

neutralise
agglutinate
opsonize
activate complement
improve phagocytosis
ADCC
degranulation

130
Q

antibody neutralisation

A

bind to bacteria/virus/toxin surface
prevent cell receptor interaction/ pathogen uptake by target cells
prior to uptake and destruction by macrophages

131
Q

direct opsonization

A

binding of antibody constant region to phagocyte receptors

132
Q

indirect opsonization

A

increase complement (C3b) deposition on pathogen and binding to complement receptors (CR1)

133
Q

complement activation

A

classical pathway
antigen-antibody complex binds C1qrs
act on C4/C3 > C3 convertase

134
Q

ADCC

A

antibody dependent cellular cytotoxicity
binding of antibodies by FcR inducing degranulation
lyses target cells#
*NK cells

135
Q

degranulation

A

eosinophils attack schistosome larva in serum presence

136
Q

degranulation via Fc receptors

A

degranulation of mast cells
killing by NK cells/ eosinophils

137
Q

fusion of B cells w B cell tumour line

A

hybridoma generation > unlimited supply of monoclonal antibody

138
Q

monoclonal antibody use in the lab

A

ELISA (enzyme-linked immunosorbent assay)
lateral flow test
antigen detection

139
Q

antibody use in the lab

A

western blotting (protein identification/ establishment in cells)
immunofluorescence
flow cytometry

140
Q

types of chains in antibody

A

kappa
lamda

141
Q

regions of antibody

A

variable regions (antigen binding site)
constant regions
12 domains

142
Q

domains

A

compactly folded globular units within proteins
functional units
~110 A.A. w intra-chain disulphide bridge

143
Q

Ig superfamily

A

T cell receptor
MHC molecules
cell adhesion molecules
signalling molecules
(2 beta strands and intra-chain disulphide bridge)

144
Q

hypervariability regions

A

in H and L variable regions
3

145
Q

V domain

A

hypervariable/ complementarity-determining regions
3 HV loops on each H/L chain
6 CDRs (antigen-binding sites)
less variable framework for other CDR loops

146
Q

C domains

A

control effector function of Ig
5 heavy chain isotypes determining size, structure and function of C region
mu/ delta/ gamma/ epsilon/ alpha

147
Q

antibody valency

A

quantity of antigen binding sites
differing isotypes and valencies

148
Q

IgM

A

macroglobulin pentamer
covalently bound to J chain
MW 900,000
found in blood
1st isotype produced
mu / 5 domains
low affin/ high avidity

149
Q

IgM locations

A

on B cell surface during B cell development
in blood

150
Q

IgM functions

A

Ig produced v rapidly
complement activation
agglutination
primary response
pathogen protect

151
Q

IgD

A

delta chain
4 domains
long hinge
BCR during B cell development
low conc in serum

152
Q

IgG

A

gamma chain
4 domains
most prevalent
^ in secondary responses
4 subclasses IgG1-4

serum location

153
Q

IgG functions

A

complement activation
opsonization
antibody-dependent cell cytotoxicity
crosses placenta for unborn protection

154
Q

IgA

A

monomer in serum
dimer in secretions
bound to J chain/ secretory component alpha chain> 4 domains
2 subclasses: 1(serum) 2 (secretions)

155
Q

IgA functions

A

mucosal membranes
microbial adherence inhibition
neutralise toxins/ pathogens
prevent commensal bacteria entry to bloodstream
neonate intestinal production

156
Q

IgE

A

5 domains
epsilon chain
binds w high affin to FCRepsilon on mast cells/ basophils
> vasoactive/ inflam mediator release
ADCC/ helminth/ protozoa infection
allergy role
induces eosinophils/ basophils to release histamine/ proteases

157
Q

anaphylaxis

A

^ histamine release /TNF alpha/ vasodilation
epinephrine epipen
^vasoconstriction/ blood glucose levels

158
Q

Ig in brain

A

devoid

159
Q

IgG locations

A

blood mainly
extracellular fluid
foetus receives from mother

160
Q

IgM locations

A

blood

161
Q

IgA locations

A

monomeric in extracellular fluid
dimeric in secretions

162
Q

IgE locations

A

mast cels below epithelial surfaces

163
Q

B cell isotypes of Ig production

A

B cell formation> IgM/IgD BCRs and then IgM/D antibodies
isotype switch w progression via irreversible DNA recombination

164
Q

main functions of T cells

A

intracellular infection control
key regulators of activities of other cells
immune memory

165
Q

cellular specific immunity

A

transferred with cells
cell-associated antigen recognition
T lymphocyte mediated

166
Q

T cells

A

use TCR to recognise pieces of antigen on cells generated by enzymatic processing
or histocompatibility complex molecules

167
Q

T cell function initiation

A

direct killing of cells displaying Ag
alert/help other cells of immune system

168
Q

TCR

A

T cell antigen receptor
heterodimer w alpha/ beta chains linked by disulphide bridge
V and C region per chain
hydrophobic trans-membrane region on each chain w short intracellular tail

169
Q

T cell vs B cell receptor

A

BCR secreted as antibody recognising native extracellular Ag
TCR not secreted recognizing pieces of Ag on cell surfaces as MHC molecule complexes

170
Q

MHC class I

A

expressed by nearly all cell types infected with intracellular pathogen
usually express CD8, kill infected cell via apoptosis

171
Q

MHC class II

A

expressed by specialized immune cells
allows detection of extracellular Ag captured by specialized immune cells (APC)

172
Q

dendritic cells

A

APC initiating acquired immune responses
exogenous antigen transport to secondary lymphoid tissue

173
Q

MHC II recognition

A

CD4+ T cell activation to “help” other cells > specific acquired immune response

174
Q

cellular immunity

A

transferred w cells
cell-associated antigen recognition
T lymphocyte mediation

175
Q

MHC

A

major histocompatibility complex
present processed antigen pieces on surface of nucleated cell
HLA (human leukocyte antigens) class I molecule

176
Q

TCR recognition outcomes

A

direct killing of infected cells displaying Ag pieces
alert/ help other immune cells

177
Q

TCR structure

A

heterodimer
alpha /beta chains linked by disulphide bridge
V (Ag interactor) and C region of each chain
hydrophobic transmemebrane region and short intracellular tail

178
Q

Ag recognition in B vs T cells

A

BCR secreted as antibody/ native extracellular Ag recognition
TCR not secreted/ recognises Ag pieces n surfaces as MHC

179
Q

MHC class 1 molecule

A

allows detection of any cell infected
T cells recognising express CD8 > apoptosis of infected cell

180
Q

CD8+ cells

A

cytotoxic T cells

181
Q

MHC class 2 molecule

A

allows detection of extracellular Ag captured by specialized immune cells > APC
CD4 T cell activation/priming

182
Q

dendritic cells

A

APC initiating acquired immune responses > exogenous antigen transport to secondary lymphoid tissue

183
Q

activated CD4 cells

A

Th cells (helper function)
via cell-cell interactions/ secretion of cytokines
different subsets based on cytokines

184
Q

naive Th cells

A

leave thymus to secondary lymphoid structures
polarization upon MHCII recognition

185
Q

CD4 Th1

A

activate macrophages
help kill intracellular pathogens
NK cell activation
more Th1 cells produced

186
Q

CD4 Th2

A

kill extracellular parasites
recruit eosinophils/ mast cells/ basophils
produce cytokines for B cell class switching to IgE class switch induction
more Th2 produced

187
Q

CD4 Tfh

A

help B cells class switch to plasma cells
activate antibody secretion

188
Q

CD4 Th17

A

help kill fungi
recruit neutrophils
promote antimicrobial peptide production
inflammation/ anti-microbial immunity at epithelial/ mucosal barriers

189
Q

CD4 Treg

A

inhibit unwanted immune responses
inhibit/ regulate T cell activation
prevent autoimmunity

190
Q

MHC structure

A

heterodimer alpha chain (a1/a2) 2 helices
8 stranded Beta sheet binding peptides
MW 44kDa
HLA-A/B/C have own alpha chain pairing w beta 2 microglobulin

191
Q

3 class 1 genes/ molecules

A

HLA-A
HLA-B
HLA-C
all pair w beta 2 microglobulin MW 12,000

192
Q

MHC class II

A

specialized APC expression
heterodimer alpha (34kDa) and beta (29kDa)
3 types> HLA-DR/ HLA-DQ/ HLA-DP

193
Q

MHC class II structure

A

alpha1/ beta1 domains form alpha helix and 8-stranded beta-sheet

194
Q

genes encoding MHC

A

clustered to form large genetic region/ complex
class I: HLA-A/HLA-B/HLA-C
class II: HLA-DRA/B HLA-DQA/B HLA-DPA/B
amino acid polymorphisms common and clustered within grooves

195
Q

endogenous acquisition of peptides

A

cytoplasmic proteins (from intra pathogens/ normal cellular proteins)
processed and presented by MHC class I molecules

196
Q

exogenous acquisition of peptides

A

proteins outside cells (extracel pathogens/normal proteins)
processed and presented by MHC class II

197
Q

MHC class I molecule peptide loading

A

cytoplasmic protein synthesis > cleaved to peptides by proteasome
transport into ER by TAP complex
assemble w newly synthesised MHC class I molecules > cell surface transport

198
Q

MHC class II molecule peptide loading

A

APC ER class 2 molecule synthesis w invariant chain > moves from ER to endocytic pathway > exogenous proteins into endocytic pathway> loading and transport to cell surface

199
Q

class II molecule invariant chain function

A

blocks groove
prevents MHC class II binding peptides present in ER

200
Q

pMHC complex recognition

A

initiates intracellular signalling cascade
via CD3 complex
ITAM (immuno receptor tyrosine-based activation motif)

201
Q

MHC recog by T cell stabilisation

A

by co-receptors CD8/CD4
MHC II > CD4

202
Q

binding of peptides by MHC

A

single peptide at time
broad specificity
polymorphic residues in peptide-bonding domains affect specificity
differences affect immune response

203
Q

MHC polymorphic genes

A

graft rejection
genetic influence on some disease

204
Q

MHC molecule expression

A

can be-upregulated/ induced on other tissues
co-dominant

205
Q

course of infection

A

local infection epithelium penetration> local infection of tissues> lymphatic spread> adaptive immunity

206
Q

pathogenicity

A

symptoms of infectious disease caused directly by pathogens/ indirectly by uncontrolled immune responses

207
Q

pathogenic mechanisms of tissue damage

A

exotoxin production
endotoxin
direct cytopathic effect

208
Q

tissue damage examples

A

infectious agent
immunodeficiency
vaccination
immunopathology
hypersensitivity
tumour immunology

209
Q

leprosy infectious agent

A

mycobacterium leprae
intracellular bacteria
granulomatous lesions
nasal droplet/ armadillo spread?

210
Q

tuberculoid leprosy

A

low infectivity
low levels
local/ granulomous inflammation
peripheral nerve damage
normal serum immunoglobulin levels/ T-cell responsiveness

211
Q

cytokine patterns in leprosy

A

tuberculoid > Th1 response effective
lepromatous> inappropriate Th2 response

212
Q

immunodeficiency

A

decreased ability to fight infection
primary/ secondary

213
Q

primary immunodeficiency

A

intrinsic defect in immune system
genetic/ rare

214
Q

secondary immunodeficiency

A

consequence of another condition
e.g. malnutrition/ immunosuppressive or cytotoxic drugs/ infection/ lymphoproliferative disease/ stress

215
Q

type I hypersensitivity

A

allergy
IgE reactant
soluble antigen
mast-cell activation

216
Q

GI tract immunopathology

A

^fluid secretion/ ^peristalsis
content expulsion

217
Q

eyes/ nasal passage/ airway immunopathology

A

decreased airway diameter
^mucus secretion
> blockage / congestion/ swelling/ mucus secretion

218
Q

blood vessel immunopathology

A

^blood flow/ permeability

219
Q

Type II sensitivity

A

IgG/ IgM mediated red blood cell destruction

220
Q

type III sensitivity

A

systemic lupus erythematosus
autoantibodies to DNA/ nuclear Ags
immune complex formation and susceptible site deposition
> glomerulonephritis/ rash/ arthritis

221
Q

Type IV sensitivity

A

organ-specific autoimmune disease
insulin-producing beta cells in pancreas
autoreactive effector T cell mediation
no insulin/ blood glucose^/death

222
Q

IgG to self-antigens

A

complex formation
cause inflammation

223
Q

autoimmune disease possible causes

A

loss of self-tolerance
^western culture frequency
more common in females

224
Q

common autoimmunity diseases

A

rheumatoid arthritis
lupus
Crohn’s disease
multiple sclerosis
T1 diabetes

225
Q

immunotherapy

A

activating immune system ^anti-tumour responses
antibodies as therapeutics to bind to tumours (specific-killing)
block activation signals leading to autoimmune responses

CMB1003- Microbiology and immunology (3 decks)

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