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

immunology (6) (Rob Spooner) Flashcards

(70 cards)

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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
toll-like receptors TLR4 TLR5 TLR9 function
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
26
granulocytes agranulocytes
neutrophils and eosinophils granules in cytoplasm (lysosomes and secretory vesicles) macrophages - but then mature to granulocytes
27
neutrophils
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
28
why are neutrophils short lived?
because they suicide
29
macrophages
``` monocytes mature to macrophages big, large nucleus longer lived remove dead damaged cells and can ingest large MOs communicate with adaptive immune system ```
30
eosinophils
work in gangs and collectively eat - coat parasite and destroy modulate allergic inflammatory responses
31
phagocytes have ....... receptors on cell surface and they...
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
what happens when any ligand binds to receptors on phagocytes (antibody or complement receptors)
activation of phagocytes - inflammation - killing - actin polymerisation
33
actin polymerisation
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
lysozymes
degrade bacterial cell wall (breaks bonds in peptidogylcan)
35
addition of sialic acid
to capsule components | avoids complement attack and engulfment
36
inflammation
blood vessels dilate swelling accumulation of complement activates TLRs in macrophages so secrete cytokines that attract neutrophils so amplify inflammation
37
dsRNA
intermediate in virus lifecycle | we make little of it so can detect viruses by this
38
interferons autocrine paracrine
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
ssRNA nuclease
destroy own mRNA so shut down protein synthesis can't make surface proteins so look foreign signals trouble
40
immunoproteasome
protealytic | destroy viral proteins
41
why do foods taste weird when you're ill?
interferons can alter structure of taste buds so change tastes
42
natural killer cells
counts grooves in receptors | viruses down regulate display of receptors so attract natural killers and cause apoptosis -persuades death
43
apoptosis
``` signals condense chromatin cytoplasmic condensation cytoplasm and nucleus fragmented phagocytosis neighbouring cells phagocyte too ```
44
antigen immunisation
anything an adaptive immune system can recognise present harmless form to immune system
45
adjuvant
enhances body's immune response to antigen | activate innate system that trains adaptive system
46
where are T cells when they are stem cells (before they mature)?
in bone marrow in adults and liver in fetus
47
how long does clonal expansion take?
a week
48
TCR
T-cell receptor
49
T-helper
activate macrophages, dendritic celles, B cells | maintain T-cytotoxic, amplify innate system
50
how do T-helper cells maintain T-cytotoxic activity?
by secreting cytokines | so amplify innate system
51
T-regulatory
inhibit function of T-helper and T-cytotoxic, dendritic cells turn off immune system
52
T-cytotoxic
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
granzyme
convert procaspase into active caspase so cleavage and cell death caspase induces apoptosis
54
difference between B cells and T cells
B cells recognise antigen by themselves while T cells recognise antigens on APCs
55
antibody structure and properties
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
5 classes of antibodies
``` IgM IgD IgG IgA IgE ```
57
IgM
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
IgD
developmental marker B cell receptor after migrated to lymphoid tissue recognise same antigens as IgM
59
opsonisation
coat target with IgM/complement so recognise by macrophages
60
IgG which domains do what?
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
passive immunity
antibodies secreted into breast milk
62
IgA
dimeric 2 antibodies joined by J chain secretory component - into mucosal surfaces also in breast milk hardly any N-glycans so very flexible
63
IgE
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
class switching
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
antibody antigen binding site
made from variable-light and variable-heavy domain interactions
66
N-glycans
complex carbohydrates added to asparagine residues during folding prior to secretion large so hold domains apart allowing exposure of functional motifs
67
clonal deletion
lymphocytes that react inappropriately with self-antigens are destroyed
68
3 antibody genes
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
affinity maturation | and evolution of high affinity antibodies
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
somatic hypermutation
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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