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pom last minute stuff > immunology > Flashcards

immunology Flashcards

1
Q

rna virus enzyme

A

reverse transcriptase

transcribes single-stranded RNA into DNA

allows integration into host dna

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2
Q

how viruses replicate

A

use hijacked host cell synthetic machinery to replicate genetic material + components

bud off or cytolysis

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3
Q

bacteria properties

A

no internal membranes
haploid
peptidoglycan walls
poorly defined cytoskeleton

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4
Q

how bacteria replicate

A

binary fission: replicate contents - elongate - divide

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5
Q

infectious dose

A

minimum number of bacteria to cause infection

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6
Q

shigella (disease, transmission, infectious dose, symptoms)

A

shigellosis = infect gut cells + destroy mucosa
fecal oral transmission
low infectious dose: 10 - 100

bloody diarrhea

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7
Q

how shigella moves without flagella

A

tricks host actin to bind cell surface protein + pull it forward

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8
Q

why is it hard to vaccinate for neisseria meningitis

A

multiple serogroups with different sugar capsules

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9
Q

neisseria meningitis transmission

A

comensal to pathogenic
community acquired

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10
Q

neisseria meningitis symptoms

A

non blanching rash (bleeding into skin)

meningitis (inflammation in brain due to bac in CSF)

septicaemia

disseminated intravascular coagulopathy (blood clots in small vessels)

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11
Q

why is clostridium difficile so hard to get rid of

A

forms spores that survive for a long time

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12
Q

why do bacteria and viruses mutate more

A

bacteria are haploid (no dominants to overcome) and rapidly divide (whole population reached quickly)

viruses have a bigger point mutation rate + mutate due to sloppy machinery

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13
Q

infections caused by fungi

A

cutaneous mycoses (skin)
mucosal mycoses (inner linings of body)
systemic mycoses (internal organs)

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14
Q

what 2 ways can fungi occur as

A

yeasts = single celled - bud off to replicate

filaments = form hyphae = multi cellular structures

or both => interchange

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15
Q

how do leishmania and plasmodium replicate

A

trophozoite formation in cells

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16
Q

why does malaria cause periodic fevers

A

parasites burst out of liver cells into the blood

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17
Q

worms life cycle

A

faecal-oral

eggs from env ingested
larvae settle in chosen env within body
grow into adults
eggs released in faeces

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18
Q

flukes life cycle

A

eggs ingested by snails => become adults
snails release infected form (cercaria) into water
absorbed into feet of humans
liver

schistomiasis => enlarged abdomen

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19
Q

primary vs secondary lymphoid organ

A

primary = where lymphopoiesis occurs
(thymus, BM, foetal liver)

secondary = where lymphocytes interact with antigens/other lymphocytes => activation + differentiation
(spleen, lymph nodes, appendix, mucosal associated lymphoid tissue)

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20
Q

function of CD4 + CD8

A

helper => release cytokines that guide B + other T cell responses

cytotoxic => actively kill foreign antigen expressing cell

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21
Q

adaptive immune response

A

specific - many T/B receptors
memory - rapid expansion in secondary encounter

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22
Q

cytokines

A

signalling molecules that slow down or speed up immune response

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23
Q

foetal vs adult bone marrow

A

f: cellular marrow
a: lots of fat present

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24
Q

red vs yellow marrow

A

r: HSC - outer
y: fat store - middle

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25
Q

t-cell vs b-cell maturation

A

thymocyte migrates to thymus from BM to mature

b-cells mature in bone marrow

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26
Q

repertoire

A

range of genetically distinct BCR+TCR in given host

larger = more pathogens recognised

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27
Q

stepwise selection of T

A

positive: can T cell signal? - see MHC?

negative: does T cell self-react => selective apoptosis

final selection + exit

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28
Q

thymic involution

A

shrinking of thymus with age
change in structure + reduced mass

begins at 20ish => all new cells made by then

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29
Q

layers of lymph node

A

marginal sinus
lymphoid follicle - where B found
germinal centre
t cell area - where T found
medullary sinus

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30
Q

parts of spleen

A

red pulp = RBC production
white pulp = WBC production

distinct B-cell + T-cell regions + germinal centres

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31
Q

germinal centre

A

anatomically restricted site in lymph node where B cells mutate + are selected to generate antibodies

(affinity maturation + somatic hypermutation)

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32
Q

gut associated lymphoid tissues

A

type of epithelial barriers

peyers patches + tonsils

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33
Q

peyers patch

A

secondary lymphoid tissue of gut that samples antigen from intestinal lumen + deliver it to APCs

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34
Q

tonsils

A

pharyngeal, tubular, palatine + lingual

form waldeyer ring in oral cavity

pathogens from food neutralised

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35
Q

how does right cell meet antigen (specific BCR/TCR)

A

lymph fluid rapidly drained between all secondary lymph organs => antigen brought here + meets right t-cell

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36
Q

excavation of T cells into lymph nodes

A

selectin binding (PNAd)

integrin binding (LFA-1 to ICAM) in high endothelial venule

transmigration into lymph node

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37
Q

antibiotic

A

antimicrobial agent made by microorganisms => kills/inhibits other microorganisms

is selectively toxic

normally made from soil dwelling fungi or bacteria

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38
Q

bacteriostatic vs bactericidal

A

static = stops bacterial growth
cidal = kills bacteria

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39
Q

antiseptic

A

prevents infection by killing or inhibiting microbes

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40
Q

prontosil
(what is it, what does it treat)

A

first sulphonamide antibiotic

treats : UTI, resp, bacteraemia, prophylaxis in HIV

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41
Q

aminoglycosides
(type, target, e.g.)

A

bactericidal

target 30S ribo subunit => no protein synthesis or dna proof reading => membrane damage as proteins x functional

gentamycin, streptomycin

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42
Q

rifampicin
(type, target, effect)

A

bactericidal

targets RpOB subunit of rna polymerase => no dna synthesis

secretions => orange/red

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43
Q

vancomycin
(type, target, why not used much?)

A

bactericidal

target lipid 2 component of wall biosynthesis + wall crosslinks via D-ala residues

toxic if too much

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44
Q

linezolid
(type. target, bacteria type)

A

bacteriostatic

inhibits protein synthesis => binds 50S subunit of ribosome

gram positive only

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45
Q

daptomycin
(type, target, why not used much?)

A

bactericidal

targets bacterial cell membrane of gram positive

too much = toxic

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46
Q

beta lactams
(type, target, e.g.)

A

bactericidal

inhibit peptidoglycan synthesis => cell wall not made

penecillin, methicillin

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47
Q

macrolides
(type, target, bacteria, e.g.)

A

bacteriostatic (cidal if high dosage)

targets 50S ribosome subunit - stop amino acyl transfer so polypeptides not made

gram + and some g -

erythromycin, azithromycin

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48
Q

quinolones
(type, target)

A

bactericidal

targets gram +ive topoisomerase IV & gram -ive DNA gyrase

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49
Q

when does antibiotic resistance occur

A

if bacteria can grow beyond breaking point (the minimal inhibitory concentration of antibiotic)

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50
Q

mechanisms of antibiotic resistance [4]

A

altered target site => alt gene for target or gene encoding target altering enzyme

inactivation of antibiotic => enzyme degradation or alteration rendering it ineffective

altered metabolism pathway => increased substrate to outcompete ab or switch metabolic pathways so enzyme not needed

reduced drug accumulation => decreased penetration of antibiotic into cell or increased efflux

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51
Q

sources of resistance genes

A

plasmids - extrachromosomal circular dna - selection for one gene in plasmid maintains resistance for all

transposons - integrate into chromosomal dna - allow gene transfer from plasmid to chromosome + vice versa

naked dna - dna from dead bacteria released into environment

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52
Q

ways that bacteria spread resistance

A

transformation (uptake of extracellular dna)
phages (virus infects bac)
conjugation (bacteria sex)

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53
Q

ways to lower resistance

A

phage antibiotic combination therapy
modification of existing antibiotics
inhibitor + antibiotic combination

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54
Q

broad spectrum antibiotic

A

effective against both gram +ive and gram -ive bacteria

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55
Q

conditons caused by fungi

A

allergy, mycotoxicoses if ingested, mycoses

(ergosterol in fungi instead of cholesterol)

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56
Q

bacteria diagnosis order

A

microscopy = type (G+/-)

culture = species

sensitivities = treatment

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57
Q

G+ vs G-

A

G+ => 1 outer membrane w/thick peptidoglycan

G- => 2 outer membranes w/thin peptidoglycan inbetween

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58
Q

why G+ purple

A

thick peptidoglycan holds crystal violet + iodine stain => G+ = thick pptg layer

gram negative = stained by safranin (pink)

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59
Q

gram staining order

A

crystal violet

iodine

alcohol - tightens peptidoglycan

safranin

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60
Q

haemolytic activity test
(differentiation, test for?, results, process)

A

which G+ (staphylo, entero or streptococcus)

tests capacity to produce haemolysins

gamma = none
alpha = partial (transparent)
beta = complete (opaque - green)

agar colony => steak on rbcs => intubate overnight => assess

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61
Q

lactose fermentation
(differentiation, test for?, results, process)

A

tests difference in pH of G-ive bacilli to see if they are lactose fermenter or non

place on MacConkey agar - containing bile salts, crystal violet and lactose

red = lactose fermenter
colourless/yellow = lactose non-fermenter

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62
Q

catalase test
(differentiation, test for?, results, process)

A

if bacteria produces catalase or not => staph produces while strep does not

loop of back placed in hydrogen peroxide => if bubbles = catalase +

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63
Q

coagulase test
(differentiation, test for?, results, process)

A

s.aureus (produces coagulase) vs other staphylococcus (dont)

bacteria on slide => plasma added => 15 sec => rotate

if clumps seen => coagulase +ive

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64
Q

2 types of antibiotic sensitivity tests

A

zone of inhibition

E-Test

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65
Q

how is E test different to zone of inhibition

A

measures minimum inhibitory conc for specific antibodies => exact value

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66
Q

benefits of an adaptive immune system

A

stops repeat immune response
improves innate response
limits response to site of infection
has memory
shorter recovery time in reinfection

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67
Q

secondary response

A

rapid + heightened
less severe re-infection
antigen specific T/B lymphocytes present

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68
Q

antigen

A

molecule inducing adaptive immune response

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69
Q

epitope

A

region of antigen that binds to TCR or BCR

TCR => linear epitope on MHC
BCR => structural epitope

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70
Q

clonal expansion

A

t-cell interacts with foreign molecule
activated
multiple copies of same lymphocyte made w/same receptors

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71
Q

solution to antigen diversity issue (not enough genes in human body to code for so many variations)

A

immunoglobulin gene reassortment => BCR chains are encoded by different multi gene families on different chromosomes => brought together in maturation

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72
Q

MHC

A

TCR => variable region made by gene reassortment which only recognises antigen fragments in MHC context

MHC bind peptide fragments from pathogens + display on surface

not needed for B-cell activation - only bind soluble antigen

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73
Q

intra vs extracellular MHC/TCR interactions

A

extracellular = endosome

intracellular = cytosol

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74
Q

MHC class 1

A

beta macroglobulin + 1 variable alpha chain

on all nucleated cells

CD8 binds alpha 3 domain

(intracellular pathogen so processed in cytosol + presented on 1)

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75
Q

MHC class 2

A

2 chains - alpha + bet

only on professional APCs

CD4 binds beta 1 domain of MHC 2

(extracellular pathogen so processed in endosome + presented on 2)

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76
Q

genetic background of MHC

A

polygenic - more than 1 gene encodes

3 MHC 1 + 3 MHC 2 loci

encoded by HLA genes

codominant

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77
Q

th17

A

pro-inflammatory

control bacterial/fungal infections

cytokines: IL17, 23 + 6

78
Q

th2

A

pro-allergic

boost multicell response

IL4, 5 + 13

79
Q

t-reg

A

anti-inflammatory

limit immune response

IL 10 + TGF-beta

80
Q

th1

A

pro-inflammatory

boost cellular immune response

interferon gamma, tumour necrosis factor, IL12

81
Q

tfh

A

pro-inflammatory

IL21

82
Q

apoptosis

A

nuclear dna fragmentation

perforin from CD8 polymerise + form pores in cell => granzymes enter + kill cell

83
Q

3 roles of antibodies

A

neutralisation => prevent bacterial adherence

opsonisation => promote phagocytosis

complement activation => enhance opsonisation + lyse bacteria

84
Q

how b cells make antibodies

A

thymus dependant => need t-helper => all Ig classes made => has memory

thymus independent => needs only microbial constituents => no memory => only IgM made

(independent: polysaccharide with repetitive structure crosslinks BCR => second signal from microbial PAMP)

85
Q

B-cell activation by T-cells

A

BCR recognises antigen

antigen internalised + degraded into peptides

peptides associate with self MHC 2 + expressed

recognised by CD4 + activated => plasma

86
Q

why must immune cell be regulated

A

too much response = excess lymphocytes activation + tissue damage

may have inappropriate response against self

87
Q

autoimmunity
(what is it, why it occurs, by what)

A

IR against self antigen => immune mediated inflammatory disease

usually when control mechanisms fail => IR inappropriately directed or controlled

by both T cells and antibodies

88
Q

allergy

A

harmful IR to non-infectious agent = tissue damage + disease

IgE + mast cells = immediate
T-cell = delayed

89
Q

hypercytokinemia + sepsis

A

too much IR => often positive FB

triggered by pathogens entering wrong compartment (sepsis) or failure to regulate response to right level

90
Q

cell mediated immunity steps

A

infected cell => DC collects material
presents on MHC
MHC - TCR on naive T => effector

effector can now recognise antigen + carries out function
becomes memory

91
Q

self limitation

A

when immune response eliminates antigen => decline in response as first signal for lymphocyte activation is eliminated

92
Q

3 signals required to elicit immune response

A

antigen recognition

co-stimulation (protein interactions on cell surface of APC, T cells and B cells)

cytokine release

93
Q

3 possible outcomes at the end of an immune response

A

resolution - no tissue damage, returns to normal - phagocytosis of debris by macrophages

repair - healing with scar tissue + regeneration - fibroblasts and collagen synthesis

chronic inflammation - active inflammation and attempts to repair damage ongoing

94
Q

immunological tolerance

A

specific unresponsiveness to an antigen that is induced by exposure of lymphocytes to that antigen (e.g. self)

95
Q

central tolerance

A

destruction of self reactive T/B cells BEFORE entering circulation

eliminated or made harmless in generative organs as part of maturation process

96
Q

t-cell repertoire in thymus vs blood

A

thymus = before central tolerance = some may be self reactive

blood = shouldn’t have any self reactive

97
Q

b-cell selection in bone marrow (central)

A

immature B cells encounter antigen which can crosslink their IgM = apoptosis triggered

(shouldn’t have foreign proteins in bone marrow)

98
Q

fate of self reactive cells

A

apoptosis

made harmless:
t => cd4 develop into t-reg
b => receptor editing - change to receptor

99
Q

T cell selection in thymus

A

useless - doesn’t bind to any self-MHC = death by neglect (apoptosis)

dangerous - binds to self-MHC too strongly = apoptosis triggered - negative selection

useful - binds to self-MHC weakly → signal to survive - positive selection

100
Q

how can a T-cell developing in the thymus encounter MHC bearing peptides expressed in other parts of the body

A

AIRE - specialised transcription factor

allows thymic expression of genes that are expressed in peripheral tissue

promotes self tolerance - t-cells exposed to all self antigens within thymus

mutation/non-existent = multi organ auto immunityn

101
Q

peripheral tolerance

A

destroy or control any self reactive T or B cells which do enter the circulation via anergy, apoptosis or suppression

102
Q

3 pathways that a B cell can go into after maturation

A

antibody production
memory cell
affinity maturation

103
Q

affinity maturation

A

B cells change antibody after leaving BM via small subtle point mutations (from somatic hypermutation)

improves antibody quality - stronger binding antibodies stay + weak = lost

improves immune response each time infected by same antigen

exposure to self-antigens can make them less tolerogenic

104
Q

anergy (P-tolerance)

A

mech of peripheral tolerance

self antigens don’t make co-stim molecules
T-cell binds self - not co-stimulated => not activated
becomes anergic

105
Q

ignorance (P-tolerance)

A

self ag = at too low conc to reach threshold for T-cell triggering

occurs at immunologically privileged sites e.g eyes, brain, placenta, foetus as no complementary T-cells can enter

106
Q

antigen induced cell death (P-tolerance)

A

continual recognition of self ag = expression of self (Fas) ligand => apoptosis

107
Q

mechanism of t-regulatory cells

A

cytokine release - IL10 (coded for by FoxP3 TF)

inactivation of dendritic cells/responding lymphocytes

IL10 also - blocks pro-inflammatory cytokine production + decreased macrophage function

108
Q

how do different pathogens each elicit a different response

A

pathogen determines TF made by naive CD4 which determines t-helper type which determines cytokines released and therefore the response

109
Q

how immune system detects so many bacteria

A

evolved to detect common features that overlap in most bacteria

110
Q

opsonisation

A

how pathogens are marked for phagocytosis

111
Q

neutrophil action

A

opsonisation of bacteria - complement activated

neutrophil recruitment (endothelial activation + up-regulation of receptors)

adhesion to endothelium via ICAM

transmigration across BV to infection site

neutrophil priming => chemotaxis

activation => phagocytosis, inflammation, degranulation

112
Q

what happens in antibody opsonisation

A

ab binds bacterial ag => complement deposition => phagocytosis

113
Q

classical pathway of complement activation

A

Fab region of ab bound to bacteria

Fc region binds C1q region of C1

C1: C4 => 4a + 4b
C1: C2 => 2a + 2b
C4bC2b = C3 convertase

complex: C3 =>3a + 3b
C4b2b3b = C5 convertase

complex: C5 => 5a + 5b

5b + 6 + 7 + 8 + 9 = membrane attack complex => penetrate pathogen membrane + destroy

114
Q

how does C3b directly help phagocytosis

A

opsonin

binds anti-phagocytic bacterial capsule so phagocyte easily binds + digests

115
Q

how is the lectin binding pathway different to the classic

A

manose = sugar on bacterial cell wall

binds manose binding lectin protein instead of ab

(=> C4 + C2 activation e.t.c)

116
Q

what is the alternate complement pathway

A

some C3 always => 3a + 3b

if bac encountered => Factor B from blood binds C3b on bacterial surface

Factor D: B => Ba + Bb

C3bBb = C3 convertase => C5 convertase => MAC etc

117
Q

how do bacteria evade antibody opsonisation [4]

A

capsule on bacterial surface => hide antigen structure so it cant be detected

new surface proteins => bind antibody in wrong direction (Fc not Fab) = cant be opsonised

protease production => cleave or modify antibodies => no opsonisation

antigenic variation => rapid change of antigen when antibody present

118
Q

how is complement opsonisation evaded by microbes

A

degradation of C3 => no C3 convertase etc

inhibited => bacterial protein inhibits C3 + C5 convertase formation = no C3b deposition or C3a formation or C5a formation

negative regulators => recruited to surface - complement inactivated

proteases cleave complement components/acquire complement regulators

119
Q

pathogen recognition receptors

A

on neutrophils

directly detect bacteria => ag binds => priming + activation

3 types:
toll like (conserved microbial products)
c-lectin (microbial carbohydrates)
FPR (formylated peptides)

120
Q

neutrophil receptors that indirectly detect bacteria (immune receptors)

A

Fc receptors detect antibody opsonised microbes

complement receptors

121
Q

receptors modulating neutrophil function
(activatory receptors)

A

cytokine receptors - detect signals from other immune cells or other cells in body

chemoattractant receptors - all neutrophil migration towards sites of infection

122
Q

activatory vs inhibitory receptors

A

enhance vs supress immune cell activity

123
Q

how bacteria evade neutrophil action

A

inhibit chemotaxis by inhibiting chemotactic receptors/chemoattractants

inhibit phagocytosis

kill neutrophils directly

124
Q

how bacteria kill neutrophils

A

toxins bind membrane => induce lysis

125
Q

IgG vs IgM vs IgA

A

M = recent infection indicator

G = more effective antiviral

A = protects mucosal surfaces

126
Q

resolution of viral infection

A

elimination of virus + virus producing cell

127
Q

how do rhinoviruses escape antibody recognition

A

hundreds of ag distinct serotypes

128
Q

how does HIV escape antibody recognition

A

multiple clades or quasi species

129
Q

how do hep B + ebola escape antibody recognition

A

encode secreted surface antigens => mop up antibodies

130
Q

how does dengue escape antibody recognition

A

4 serotypes

when infected with 2 => ab independent enhancement

haemorrhagic fever

131
Q

how does influenza escape antibody recognition

A

mutates yearly

132
Q

interferon

A

small protein made by virally infected cells when foreign viral molecules detected inside

released => binds IFN receptors => initiates antiviral state of cellat it binds

133
Q

what is the antiviral state

A

transcription of 100s of genes that block viral replication

(mrna degradation + inhibition of protein synthesis)

also activates MHC 1 => displayed on cell surface

134
Q

type 1 interferons
(types, secretion, receptor, genetics)

A

IFN alpha + beta

b = secreted by all cells, a = by plasmacytoid dendritic cell

a-R is on all tissue

1 gene codes b, 13-14 isophores of a

135
Q

type 2 interferon
(type, formation, receptor)

A

IFN-gamma

made by activated T + NK cells

IFNy-R

136
Q

type 3 interferon
(type, receptors)

A

IFN-lambda

IL28-R + IL10-B receptors on epithelial surfaces

137
Q

how HepB and influenza block IFN

A

HepB virus: inhibit IFN transcription

Influenza: makes NSI protein - counters RNA sensing + prevents polyA processing

138
Q

NK cells and IFN

A

activated by IFN-a + IL12 which then activate macrophages with IFN-y

NK target cells with less MHC + kill by releasing toxins

139
Q

dendritic cells and IFN

A

immature + plasmacytoid DCs => IFN-α + other cytokines

initiate + determine nature of CD4 + CD8 response

present antigen to CD4 T cells

140
Q

how does HIV impair lymphocyte function

A

kills CD4 + alters macrophage function

141
Q

how does Herpes Simplex Virus impair lymphocyte function

A

prevents CD8 killing

142
Q

what is anaphylaxis + what can trigger it

A

type 1 HS reaction

penecilin, other drugs, venom, peanuts

143
Q

histamine action on connective tissue

A

(released by mast cells)

vessel dilation

increased blood to surface

increased fluid movement out of bloodstream = oedema

144
Q

histamine action around mucosae

A

airway constriction

SM contraction in intestine walls

145
Q

acute allergic reaction

A

wheezing
urticaria (rash = mast cell causes vasodilation + oedema)
sneezing
rinorrhea (runny nose)
conjunctivitis (inflammation in eyes)

146
Q

anaphylactic shock

A

blood vessel dilation = low BP = decreased organ function

adrenaline given => constricts BVs + redirects blood to organs

147
Q

anaphylaxis drugs

A

antihistamines + anti-inflammatory corticosteroids

148
Q

vaccine

A

stimulates immune system without harm or side effects => provides immunological memory

149
Q

ideal vaccine

A

safe, easy admin, 1 dose no needle, stable, all variants targeted, lifelong immunity

150
Q

main functions of vaccine

A

prevent entry => macrophages that engulf pathogens

boost immune response => antigens in vaccine activates CD4

kill infected cells

151
Q

R0

A

number of cases that 1 case of viral infection generates over infectious period

<1 = infection dies out
>1 = able to spread

152
Q

Rt

A

alteration of R0 due to vaccine

153
Q

idea behind herd immunity

A

immune people cant pass on infection to those unable to be vaccinated

154
Q

vaccine contents

A

antigen
stabilising stuff
adjuvant - alum
water

155
Q

adjuvant

A

substance that enhances body’s immune response to an antigen

e.g alum => stores antigen at infection site, allowing dendritic cells to see it

156
Q

inactivated toxoid vaccine
(what is it, how does it work, examples)

A

(chemically inactivated form of toxin)

toxin binds cell surface receptor

endocytosis of toxin-receptor complex

dissociation of toxin - releases active chain => poisons cell

neutralising antibody blocks further binding of toxin to cell surface receptors

e.g diphtheria + tetanus

157
Q

recombinant protein vaccines
(what is it, how does it work, examples)

A

recombinant protein from pathogen

surface antigen gene isolated

insertion into another substance (e.g. yeast for Hep B virus)

modified cell produces antibodies that neutralise

e.g HepB

158
Q

conjugate vaccine
(what is it, what does it do)

A

polysaccharide coat component is coupled to an immunogenic “carrier” protein

protein enlists CD4 help to boost B cell response to the polysaccharide

(naturally, B-cells are bad at recognising bacterial coats)

159
Q

dead pathogen vaccine
(what is it, what does it do, example)

A

e.g influenza

chemically killed pathogen

induces antibody and T cell responses

160
Q

how are pathogens attenuated

A

serial passage → leads to loss of virulence factors

161
Q

live attenuated vaccines

A

viral cells replicate in situ triggering the innate response + boosts the immune response

but no disease due to no virulence factors

162
Q

type 1 hypersensitivity

A

immediate type - anaphylactic - allergy

IgE

163
Q

type 1 - sensitization

A

allergen in system = picked up by APC (DC/mac) => to lymph node (displays on MHC)

naive T binds allergen + co-stimulatory molecules => primed => Th2 - releases IL4 + 5 + 10

IL4 => B-cell class switching to make allergen specific IgE instead of M

IL5 => stimulates eosinophils

IgE binds Fc-epsilon receptor on mast cells

164
Q

type 1 - allergic reaction

A

mast cells bind antigens using new IgE => 2 or more to crosslink

degranulation

pro-inflammatory mediators (histamine) released => symptoms

Th2 + basophils recruited to inflamm site

IL2, 4 + 10 + leukotrienes released => SM contract + attract more immune cells

165
Q

type 2 hypersensitivity
(what is it, Ig, examples x4)

A

antibody mediated / cytotoxic
(normal response to non-self or abberant response to self)

IgG/M

mismatched blood transfusion
HDFN
immune thrombocytopenia (ABs against surface proteins)
graves disease

166
Q

type 2 process
(what 4 things happen)

A

IgG/M bind ag

complement activation => C3a, 4a, 5a = chemoattractants => neutrophils => degranulate + kill host cell bound to Ig

C5b, 6, 7, 8 + many 9 = MAC => cell lysis

host cell also can be phagocytosed (C3a binds => opsonised)

ADCC => antibody dependant cell mediated cytotoxicity
ag-ab complex recognised by NK (Fc) => perforin
granzymes + granulysins into pores
apoptosis - no inflammation

167
Q

type 3 hypersensitivity (process)

A

immune complex mediated

IgG

immune complexes made from Ag-Ab = normally cleaved => if not (e.g if self) - deposit in blood vessel walls

cause: tissue damage + inflammation

(rash, fever, joint pain, proteinuria, vasculitis, glomerulonephritis, arthritis

168
Q

conditions caused by type 3

A

autoimmune:
rheumatoid
MS
lupus - IgG against dna/proteins in nucleus

serum sickness:
bitten => venom => antiserum => foreign so abs made
2nd bite => immune complexes made = inflammation

169
Q

type 4 hypersensitivity

A

delayed type / t-cell mediated

no Ig

170
Q

type 4 process

A

allergen from skin picked up by DC => lymph node => presents ag on MHC 2

T helper binds via TCR + CD4 co-receptor => forms memory T-cell

allergen binds memory T:

Dc release IL12 => Th mature to Th-1 = effector

Th1 => IL2 (t-cell proliferation) + IFN-gamma (activates phagocytosis)

phagocytes => pro-inflammatory cytokines => endothelial barriers become leaky => more immune cells to area = inflammation + tissue damage

171
Q

type 4 examples

A

poison ivy
nickel reaction
hair dye reaction
measles
TB

172
Q

immunogen + immunogenicity

A

gen => antigen that can elicit IR

genicity => ability of substance to elicit IR

173
Q

hapten

A

small molecule thats not antigenic on its own but forms antigen when associated with large carrier protein

174
Q

DAMP

A

damage associated molecular patterns

molecules released due to abnormal non-apoptotic cell death => activate innate immune response

175
Q

PAMP

A

pathogen associated molecular patterns

common molecular patterns in pathogens + microbes but not in host cells

activate innate response

176
Q

PRR

A

pattern recognition receptors

detect PAMP + DAMP

177
Q

therapeutic index

A

amount of antiviral drug required to control virus vs amount causing side effect (ratio)

178
Q

virion

A

viral particles => v.small but lots of ribosomes + proteins
only seen on electron micrographs

179
Q

what is the central dogma

A

theory stating that genetic information flows only in one direction, from DNA, to RNA, to protein, or RNA directly to protein

180
Q

negative sense rna

A

complementary to mRNA

converted to positive sense by RNA-dependent RNA polymerase for translation

181
Q

rna vs dna virus

A

rna = increased mutation due to lack of proof-reading + limited genome means complex coding strategies used to make proteins

dna = large genome = gain more accessory genes that modify IR

182
Q

segmented genome virus
(what is it + what does that mean)

A

RNA separated into segments - each codes for a specific protein

allows for easy recombination/reassortment => evolution
(esp if more than one virus affects same cell)

183
Q

viral replication basics

A

attaches viral receptors on cell + enters
capsid lost
viral genome exposed
translated into proteins using cell machinery or own polymerase
replicated
cell lysis => further infection

184
Q

cytopathic effect of virus

A

changes in cell morphology

host protein synthesis shutdown + accumulation of viral proteins => lysis

viral plaques + syncytia

185
Q

detection of viruses on cultured cells - cytopathic effects

A

viral plaques => holes in cell culture due to viral infections => used to measure virus effects (plaque assays)

syncytia => viruses fuse cells around them => multi-nucleated structure => no: syn = measure of viral infection

186
Q

how to diagnose viruses

A

detect viral genome, antigen or particles

viral cytopathic effect on cultured cells - plaque/syncytia

detect antibodies to virus

187
Q

why is it hard to make antivirals

A

selectivity + specificity => hard to distinguish viral + host cell replicative mechanisms

188
Q

herpes treatment

A

acyclovir = nucleoside analogue

similar to guanosine but no OH

incorporates into viral dna + acts as chain terminator as phosphodiester bond not formed without OH

given as un-phosphorylated prodrug => only phosphorylated by viral thymidine kinase in herpes => only activated when meets

189
Q

COVID antivirals

A

remedesivir => adenosine analogue = chain terminator

dexamethasone = pro-inflamm => IR suppressed

190
Q

influenza antivirals

A

amatidine => block M2 channel on endosome so virus trapped inside

neuaminidase inhibitor => sialic acid, relenza, tamiflu => virus cant spread to other cells as bound to first host

baloxavir => inhibits PA endonucleases => inhibits viral dna replication

191
Q

Hep C antivirals

A

positive sense flavivirus

protease inhibitors
NS5B inhibitors

192
Q

what is a biological + example

A

passive immunotherapy => antibodies from a recovered individual given to patient

e.g. paliczumab => humanised mouse monoclonal antibodies => RSV in infants

pom last minute stuff (4 decks)

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