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MFMII > Antigen Processing and Presentation > Flashcards

Antigen Processing and Presentation Flashcards

1
Q

what is the most potent APC?

A

dendritic cells

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2
Q

function of dendritic cells?

A
  1. capture Ag and process into small peptides to bind to MHC
  2. present Ag to activate T cells
  3. support the functions of other cell s
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3
Q

which cells are professional APC?

A
  1. macrophages
  2. dendritic cells
  3. B cells
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4
Q

how do B cells act as APC?

A

ingest antigens and display them on MHC II to the CD4 helper cells in lymphoid tissue to generate humoral immune response

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5
Q

how do DC capture proteins/Ag?

A

endocytosis! which then binds to phagosome

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6
Q

which MHC binds to CD4

A

MHC II

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7
Q

which MHC binds CD8?

A

MHC I

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8
Q

which cells contain MHC I?

A

all nucleated cells

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9
Q

structure of MHC I?

A

3 segmented alpha chain, 1 segmented beta globulin

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10
Q

what cells contain MHC II?

A

only DC, macrophages, B cells

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11
Q

structure of MHC II

A

2 alpha chains and 2 beta chains

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12
Q

what antigens do MHC I display?

A

endogenous Ag

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13
Q

what antigens do MHC II display?

A

exogenous Ag

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14
Q

1st step of endogenous Ag processing

A

proteasome and immunoproteosome take up ubiquinated proteins to make peptides

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15
Q

when is proteasome active?

A

active in the absence of infection

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16
Q

what does proteasome do?

A

degrades cytosolic proteins that are damaged, poorly folded or no longer needed

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17
Q

what induces immunoproteosome?

A

IFN gamma that was produced by NK cells or T cells (Th1)

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18
Q

how are peptides produced by proteasome and immunoproteosome transported out of the ER?

A

TAP transports peptides across ER membrane into ER lumen via ATP

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19
Q

what occurs if there is a TAP deficiency in a patient?

A
  1. chronic respiratory infections from birth
  2. minimal CD8 response
  3. little MHC I on cell surfaces
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20
Q

what does calnexin do?

A

stabilizes construction of MHC I ALPHA chain

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21
Q

where are the alpha chain and beta 2 microglobulin chains of MHC I produced?

A

ER

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22
Q

what occurs once the B2micro chain and alpha chain come together?

A

ERp57 tapasin-Calreticulin helps it associate with TAP (so peptides can come through TAP)

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23
Q

what is the last thing that stabilizes MHC I?

A

peptide binding!

24
Q

what occurs once MHC I binds peptide?

A

tapasin is released, and signal peptide is added to the loaded MHC I to drive it to cell surface

25
Q

what does ERAP do?

A

trims oversized peptides into manageable lengths for MHC I

26
Q

what must occur first before MHC II molecules are begun to be made?

A

endosome with Ag fuses with phagosome and undergo acidification to activate acid hydrolase where peptide can be unfolded and degraded

27
Q

what function does the invariant chain do when the MHC II alpha and beta chains are generated?

A
  1. blocks MHC II peptide binding site so it doesn’t bind ER peptides
  2. stabilizes MHC II
  3. directs vesicle transport
28
Q

how is invariant chain released from MHC II?

A

cathepsin S and proteases cleave it, but leave CLIP

29
Q

what component remains bound to MHC II after invariant chain is released from MHC II?

A

CLIP (class II associated invariant chain peptide)

30
Q

what occurs once invariant chain is clipped?

A

the MHC II compartment vesicle fuses with endosome/phagolysosome with the peptides in them

31
Q

what finally removes CLIP from MHCII binding site?

A

HLA-DM removes CLIP so that peptides can bind

32
Q

what triggers HLA-DM release from MHCII?

A

right peptide binding to MHC II

33
Q

what occurs once HLA-DM is released?

A

HLA-DO binds to it so it doesn’t try and bind to MHC II again

34
Q

what effect does IFN gamma have on this process?

A

increased HLA-DM expression and increased Ag presentation which directly increases the number of MHC II molecules

35
Q

what cells can undergo cross presentation of Ag?

A

dendritic cells

36
Q

steps of cross presentation

A
  1. Ag export from phagosome to cytosol
  2. Ag transport into phagosome
  3. phagosome degradation of Ag
37
Q

why is cross presentation a thing?

A

if an antigen is presented exogenously, you want them to be killed by CD8, so you would need MHC I presentation, which is done endogenously. therefore, must uptake and degrade them so they can be shown to MHC I – for memory generation

38
Q

where do the DC live that do cross presentation

A

lymph node

39
Q

what does cross dressing actually do

A

transfer of preformed MHC peptide from the migrating DC to the Lymph node DC to present

40
Q

describe direct presentation

A

endogenous Ag binds to endogenous MHC I

41
Q

describe cross presentation

A

exogenous Ag binds to endogenous MHC I

42
Q

describe cross dressing

A

exogenous Ag binds to exogenous MHC I

43
Q

what increases alpha and beta2microglobulin and TAP expression for MHC I?

A

IFN alpha, IFN beta, IFN gamma

44
Q

what increases HLA-DM, HLA-DP, HLA-DQ, HLA-R and invariant chain?

A

IFN gamma

45
Q

how are HLA genes inherited?

A

both sets of genes are expressed, meaning that maternal and paternal genes are inherited

46
Q

benefit of HLA inheritance?

A

ensures that a greater number of pathogen derived peptides will be presented during any infection (any infection your parent has had, you have the HLA for that)

47
Q

what is linkage disequilibrium?

A

when haplotypes of HLA exist that are due to meiotic recombination events (random resistance to disease_

48
Q

how are new MHC alleles derived?

A

mutations from infections/pathogens resulting in natural selection (for survival advantage)

49
Q

what does HLA-E do?

A

is a MHC class Ib molecule that engages NK cells

50
Q

what occurs if HLA-E interacts with NKG2A or NKG2B?

A

inhibition of NK

51
Q

what occurs if HLA-E interacts with NKG2C?

A

activation of NK

52
Q

what occurs if there is a MHC class I loss on cells?

A

upregulate HLA-E and express NKG2A and NKG2B to inhibit NK so they don’t kill you

53
Q

how are fetal cells not destroyed by mother’s NK cells?

A

placental and fetal cells express HLA-G, which binds to KIR2DL4, inhibiting NK cell destruction

54
Q

what does MICa and MICb do?

A

binds NKG2D on NK cells, NKT cells, and cytotoxic lymphocytes and overrides the inhibitory signal from MHC I on NK = NK cell activation, aka activated and killing things

55
Q

what is MHC restriction?

A

where TCR recognizes Ag on self MHC’s but not on new or non-self MHC - occurs during organ transplant rejection

56
Q

what helps increase diversity of peptide binding in MHC?

A

number of AA residues in binding pocket of MHC bind, leaving other peptides to contact TCR bulge

MFMII (29 decks)

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