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Y3 Medical Micro > L2 Immune recognition > Flashcards

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

A

one chain

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

A

CD8

24
Q

what does MHC class II present to

A

CD4

25
Q

when does the T cell kill the pathogen

A

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
Q

when is the T helper cell activated

A

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
Q

what can MHCI present

A

small peptides 8-10 amino acids to CD8 cell

28
Q

what can MHCII present

A

larger at least 13 amino acid epitope to CD4

29
Q

what is the CD3 complex function

A

has activation motifs inside cell that activate T cell to carry out its effector function

30
Q

what is the CD3 co-receptor function

A

CD3 and co-receptor complex comes together to signal and activate the T cell

31
Q

where are cytosolic pathogens degraded

A

cytosol

32
Q

what peptides bind to a cytosolic pathogen

A

MHCI

33
Q

what T cell are cytosolic pathogens presented to

A

CD8

34
Q

what happens to cytosolic pathogens

A

killed - cell death

35
Q

where are intravesicular pathogens degraded in

A

endocytic vesicles

36
Q

what peptides bind to intravesicular pathogens

A

MHCII

37
Q

what T cell are intravesicular pathogens presented to

A

CD4

38
Q

what happens to intravesicular pathogens

A

activation to kill intravesicular bacteria and parasites

39
Q

where are extracellular pathogens and toxins degraded

A

endocytic vesicles

40
Q

which peptides bind to extracellular pathogens and toxins

A

MHCII

41
Q

what are extracellular pathogens and toxins presented to

A

CD4

42
Q

what happens to extracellular pathogens and toxins

A

activation of B cells to secrete Ig - eliminate them

43
Q

why do other non innate cells have MHCI

A

any cell could be infected by virus so not just innate cells with MHC I

44
Q

what happens in MHCI processing and presentation

A

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
Q

where is MHCII made

A

made in endoplasmic reticulum

46
Q

what happens to MHCII invariant chain

A

has an invariant chain bound to it, when leaves endoplasmic reticulum is cleaved in vesicle

47
Q

what is important in blood transfusion

A

need to have HLA matching in transplantation

Y3 Medical Micro (16 decks)

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