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1st year: AID > immunology (6) (Rob Spooner) > Flashcards

immunology (6) (Rob Spooner) Flashcards

1
Q

extracellular pathogens

and examples

A

bacteria, parasites, fungi

S.pneumonia
C.tetani
Sleeping sickness

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2
Q

S. pneumonia

A

Gram +ve
90 diff serotypes
only pathogenic when other infections present

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3
Q

C. tetani

A

Gram +ve
spore forming - heat resistant, on human skin
release toxins that interfere with neural impulses

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4
Q

sleeping sickness

A

protozoan (C.T brucei)
carried by Tsetse flies
can change varralleles so shift outer coat so immune system can’t recognise

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5
Q

intracellular pathogens

A

bacteria, parasites
M. leprae
L. donovani
P. falciparum

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6
Q

M. leprae

A

Gram +ve
infects macrophages and Schwann cells
leprosy

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7
Q

L. donovani

A

protozoan

infects macrophages

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8
Q

P. falciparum

A

protozoan
infects erythrocytes
malaria

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9
Q

examples of viruses

A

smallpox
influenza
chicken pox

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10
Q

flu evolution

A

recombination of RNA segments
H + N are surface spikes on flu that change
so lots strains

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11
Q

antigenic variation/shift

A

change coat e.g. malaria

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12
Q

why do we need an innate non-specific response?

A

if there’s a new pathogen, the specific response is too slow so need innate to survive first few days
1st line of defence, inherited, no memory, ancient origin

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13
Q

adaptive immune response

A

memory

slow (7-10 days), specific, somatic gene recombination generates response
only in vertebrates

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14
Q

brain immune system

A

no adaptive response so survives on the innate response

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15
Q

humoural mechanisms/immunity

A

macromolecules in extracellular fluid like antibodies
soluble-phase defence, secreted proteins in bodily fluids, immunoglobulins

innate - barriers, defensins, complement proteins
adaptive - antibodies

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16
Q

cell-mediated responses

A

lymphocytes, specialised cells,

innate - phagocytic, APC, natural killer, TLR
adaptive - APC, T cells, B cells

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17
Q

complement proteins

A

soluble proteins that activated upon infection, proenzymes

cause inflammation

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18
Q

3 lines of innate immune defence

A

barries - physical and chemical
cell-intrinsic response (phagocytosis)
speciliased proteins and cells

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19
Q

O-linked Glycans

A

sugars attached by oxygen groups

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20
Q

defensins

A 
small positively charged antimicrobial peptides that kill or inactivate pathogens
have hydrophobic (beta sheets) or amphipathic helical domains (coil)
multiple classes so target wide range of pathogens
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21
Q

PAMPs

A

innate system recognises these pathogenic molecules

e.g.
fMet - used for bacterial translation initiation, attract neutrophils
peptidoglycans from bacterial cell walls
bacterial flagellae
LPS from Gram -ve
Mannans, glucan, chitin from fungi

we don’t make any of these so we recognise it as foreign

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22
Q

how does immune system recognise PAMPs?

A

pattern recognition receptors (PRRs) - soluble receptors in blood and cellular receptors

blood receptors - complement system perform killing and aid phagocytosis
cell receptors - toll-like receptors that are membrane bound stimulate inflammation

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23
Q

lectin

A

any protein that bind to sugar

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24
Q

toll receptors

A

Drosophila trans-membrane protein
large extracellular domain with repeating motifs (leucine-rich repeats) - bind proteins and cause expression of defensins

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25
Q

toll-like receptors

TLR4
TLR5
TLR9

function

A

bind PAMPs
most on cell membrane on epithelial cells, macrophages, dendritic, neutrophils

LPS
flagellum
CpG motifs in DNA

signal to nucleus to transcribe pro-inflammatory genes and cause interferon response

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26
Q

granulocytes

agranulocytes

A

neutrophils and eosinophils
granules in cytoplasm (lysosomes and secretory vesicles)

macrophages - but then mature to granulocytes

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27
Q

neutrophils

A

polymorphonuclear leucocytes - multilobed nucleus
most common granulocyte
1st defence against bacteria
attracted to infected tissue by macrophages/cleaved complement proteins/PAMPs, and cause inflammation
abundant in blood
short lived because suicide

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28
Q

why are neutrophils short lived?

A

because they suicide

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29
Q

macrophages

A 
monocytes mature to macrophages
big, large nucleus
longer lived
remove dead damaged cells and can ingest large MOs
communicate with adaptive immune system
30
Q

eosinophils

A

work in gangs and collectively eat - coat parasite and destroy
modulate allergic inflammatory responses

31
Q

phagocytes have ……. receptors on cell surface and they…

A

toll like receptors (TLRs)
are activated when contact with a pathogen is made
they act as receptors for antibodies and for complement 3b protein if pathogen is coated in complement

32
Q

what happens when any ligand binds to receptors on phagocytes (antibody or complement receptors)

A

activation of phagocytes - inflammation - killing - actin polymerisation

33
Q

actin polymerisation

A

actin of our cytoskeleton changes so cell changes shape and wraps around target so traps it inside phagosome

granules go to actin polymerisation site and fuse with phagosome releasing acid hydrolases/defensins/lysozymes

34
Q

lysozymes

A

degrade bacterial cell wall (breaks bonds in peptidogylcan)

35
Q

addition of sialic acid

A

to capsule components

avoids complement attack and engulfment

36
Q

inflammation

A

blood vessels dilate
swelling
accumulation of complement activates TLRs in macrophages so secrete cytokines that attract neutrophils so amplify inflammation

37
Q

dsRNA

A

intermediate in virus lifecycle

we make little of it so can detect viruses by this

38
Q

interferons

autocrine
paracrine

A

group of signalling proteins called cytokines produced by white blood cells, fibroblasts, or T-cells
response to a viral infection
ability to interfere with the production of new virus particles by limiting replication and spread

work on cells that produce them
work on neighbouring cells

39
Q

ssRNA nuclease

A

destroy own mRNA so shut down protein synthesis
can’t make surface proteins so look foreign
signals trouble

40
Q

immunoproteasome

A

protealytic

destroy viral proteins

41
Q

why do foods taste weird when you’re ill?

A

interferons can alter structure of taste buds so change tastes

42
Q

natural killer cells

A

counts grooves in receptors

viruses down regulate display of receptors so attract natural killers and cause apoptosis -persuades death

43
Q

apoptosis

A 
signals
condense chromatin
cytoplasmic condensation
cytoplasm and nucleus fragmented
phagocytosis
neighbouring cells phagocyte too
44
Q

antigen

immunisation

A

anything an adaptive immune system can recognise

present harmless form to immune system

45
Q

adjuvant

A

enhances body’s immune response to antigen

activate innate system that trains adaptive system

46
Q

where are T cells when they are stem cells (before they mature)?

A

in bone marrow in adults and liver in fetus

47
Q

how long does clonal expansion take?

A

a week

48
Q

TCR

A

T-cell receptor

49
Q

T-helper

A

activate macrophages, dendritic celles, B cells

maintain T-cytotoxic, amplify innate system

50
Q

how do T-helper cells maintain T-cytotoxic activity?

A

by secreting cytokines

so amplify innate system

51
Q

T-regulatory

A

inhibit function of T-helper and T-cytotoxic, dendritic cells
turn off immune system

52
Q

T-cytotoxic

A

T-killer
kill infected cells by apoptosis
flatten against antigen and form immunological synapse, secrete perforins which punch pores in membrane and secrete granzyme to cytosol

53
Q

granzyme

A

convert procaspase into active caspase so cleavage and cell death
caspase induces apoptosis

54
Q

difference between B cells and T cells

A

B cells recognise antigen by themselves while T cells recognise antigens on APCs

55
Q

antibody structure and properties

A

light chains on outside
disulfide bonds between light and heavy chain
flexible hinge region allows crosslinks and networks

1 bind to 2 same antigens or cross link if antigen has 2 determinants
3 or more is a network - entrapped

56
Q

5 classes of antibodies

A 
IgM
IgD
IgG
IgA
IgE
57
Q

IgM

A

1st antibody B cells make - B cell receptor
5 Y-shaped antibodies held by J (joining) chain and disulfide bonds

activates C3a and C3b
is an opsonin because activates complement (aids in phagocytosis)

58
Q

IgD

A

developmental marker
B cell receptor after migrated to lymphoid tissue
recognise same antigens as IgM

59
Q

opsonisation

A

coat target with IgM/complement so recognise by macrophages

60
Q

IgG

which domains do what?

A

classic antibody structure
most abundant
neutralisation
opsonisation - phagocytes recognise tail region
secreted into milk and can cross placenta

constant domain (C) 1 and 2 bind complement components
C2 and 3 bind Fc receptors on neutrophils
C3 binds Fc receptors on macrophages and NK

61
Q

passive immunity

A

antibodies secreted into breast milk

62
Q

IgA

A

dimeric
2 antibodies joined by J chain
secretory component - into mucosal surfaces
also in breast milk

hardly any N-glycans so very flexible

63
Q

IgE

A

binds Fc receptors on mast cells/basophils/eosinophils and cause release of histamine - inflammation
receptor for eosinophils so help phagocytosis

heavily N-glycosylated - stiff so target large pathogens

64
Q

class switching

A

there is only 1 heavy chain gene that encodes all antibodies so somatic recombination of DNA occurs which removes specific parts and loops so alignment of variable heavy chain upstream to different Igs so diff chains are generated when loop taken off
primary mRNA –> mature mRNA

e.g. B cell to plasma cell

65
Q

antibody antigen binding site

A

made from variable-light and variable-heavy domain interactions

66
Q

N-glycans

A

complex carbohydrates added to asparagine residues during folding prior to secretion
large so hold domains apart allowing exposure of functional motifs

67
Q

clonal deletion

A

lymphocytes that react inappropriately with self-antigens are destroyed

68
Q

3 antibody genes

A

1 HC heavy chain gene
2 LC light chain genes (lambda and K)
so 2 versions of every antibody with lambda or K LC

69
Q

affinity maturation

and evolution of high affinity antibodies

A

antibodies in lymph nodes get better and become more specific
when activated, B cells are released or stay in lymphoid follicles but expand to germinal centres where high rate mutation in variable domains

70
Q

somatic hypermutation

A

B cells remain in follicles forming germinal centres

generate B cells with altered V domain specificity

1st year: AID (5 decks)

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