L2 Immune recognition Flashcards

1
Q

what are the two types of recognition molecules

A
B cells (B cell receptor/immunoglobulin)
T cells (TCR)
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2
Q

what is the B cell immunoglobulin structure

A

2 heavy 2 light chains, constant and variable domains at the two combining site - antigen binding
Hinge

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3
Q

how come B cell immunoglobulins move to bind to target

A

have a hinge

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4
Q

what is the T cell receptor structure

A

Alpha and beta chain has constant (close to cell surface) and variable domain – only one antigen combining site made of variable alpha and beta chain

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5
Q

what is the difference between B and T cell recognition

A

T cell cant directly recognise need info presented to them via antigen presenting cell

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6
Q

how do B cells recognise

A

surface Ig – bind directly to pathogen /antigen

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7
Q

what happens to B cell following recognition

A

B cell activated makes plasma cells = lots more Ig which all bind to the pathogen

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8
Q

how do T cells recognise

A

needs info of pathogen processed and presented to it via MHC
antigen presenting cells do this e.g. dendritic cells

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9
Q

what happens to T cell following recognition

A

effector cell activated – might be CD4 or CD8 (depends on the MHC)

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10
Q

where is there variability the variable domains

A

areas of hypervariability – variation between amino acid structure is huge = will recognise a different target
3 areas of hypervariability in heavy and light

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11
Q

how are B cells activated

A

only through B cell clustering

Ig alpha and Ig beta have capacity to signal to cell to become activated – have tyrosine receptor molecules to intracellulary activate Ig alpha and beta molecules found in conjunction with B cell receptor

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12
Q

why cant the B cell become activated by itself

A

might be a chance encounter with antigen or might bind to a target not specifically – can’t have this or adaptive response and B cells constantly activated

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13
Q

what does BCR complex clustering cause

A

lots of B cells bind to target = B cell receptor clustering

turns on Ig alpha and beta signal B cell to start making lots of antibodies

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14
Q

what is the BCR co-receptor complex

A

second signal through complement receptors binding to complement that has opsonized the pathogen

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15
Q

what is needed for B cell to make antibodies

A

BCR clustering and BCR co-receptor complex

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16
Q

what is the TCR for

A

not able to signal only there for indirect recognition via antigen presenting cell

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17
Q

what are the two classes of TCR

A

alpha beta

gamma delta

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18
Q

what are the T cell co-receptors

A

CD$

CD8

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19
Q

what is the structure of the CD4 receptor

20
Q

what is the structure of the CD8 receptor

A

one alpha one beta molecule in separate chains

21
Q

what does the helper T cell express

A

helper T cell expresses CD4 alongside T cell receptor

22
Q

what does the cytotoxic T cell express

A

cytotoxic T cell expresses CD8 alongside T cell receptor

23
Q

what does MHC class I present to

24
Q

what does MHC class II present to

25
when does the T cell kill the pathogen
virus gone into the cell on its own *infected will be in cytosol virally infected cell T cell by MHC I – bind to CD8 co receptor T cell – to kill it
26
when is the T helper cell activated
pathogen deliberately taken into cell via phagocytosis will be in vesicle T cell with CD4 co receptor will bind = helper T cell activated to help clear it
27
what can MHCI present
small peptides 8-10 amino acids to CD8 cell
28
what can MHCII present
larger at least 13 amino acid epitope to CD4
29
what is the CD3 complex function
has activation motifs inside cell that activate T cell to carry out its effector function
30
what is the CD3 co-receptor function
CD3 and co-receptor complex comes together to signal and activate the T cell
31
where are cytosolic pathogens degraded
cytosol
32
what peptides bind to a cytosolic pathogen
MHCI
33
what T cell are cytosolic pathogens presented to
CD8
34
what happens to cytosolic pathogens
killed - cell death
35
where are intravesicular pathogens degraded in
endocytic vesicles
36
what peptides bind to intravesicular pathogens
MHCII
37
what T cell are intravesicular pathogens presented to
CD4
38
what happens to intravesicular pathogens
activation to kill intravesicular bacteria and parasites
39
where are extracellular pathogens and toxins degraded
endocytic vesicles
40
which peptides bind to extracellular pathogens and toxins
MHCII
41
what are extracellular pathogens and toxins presented to
CD4
42
what happens to extracellular pathogens and toxins
activation of B cells to secrete Ig - eliminate them
43
why do other non innate cells have MHCI
any cell could be infected by virus so not just innate cells with MHC I
44
what happens in MHCI processing and presentation
proteasome degrades antigen in cytosol – pieces taken to endoplasmic reticulum MHCI load info onto cell surface = activate CD8 cytotoxic T cell phagocytosis - degraded in vesicle
45
where is MHCII made
made in endoplasmic reticulum
46
what happens to MHCII invariant chain
has an invariant chain bound to it, when leaves endoplasmic reticulum is cleaved in vesicle
47
what is important in blood transfusion
need to have HLA matching in transplantation