Adaptive Immunity, MHC, B-Cells, T-Cells (complete) Flashcards

1
Q

What are the three main ways that adaptive immunity is different from innate immunity

A
  1. instead of a limited number of receptors, lymphocytes have 1 receptor will nearly infinite possibilities
  2. delayed onset, a few days
  3. immune memory = next exposure is better/faster
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2
Q

how many type of receptors does each t cell have

A

1

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3
Q

What is the MHC

A

major histocompatibility complex

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4
Q

what are the two types of MHCs

A
class 1 antigens
class 2 antigens
(there are also class 3, but they aren't as important to immunity)
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5
Q

where do you find class 1 MHCs

A

almost all nucleated cells

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6
Q

where do you find class 2 MHCs

A

only in APCs (antigen presenting cells)

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7
Q

what do class 1 MHCs do

A

hold a peptide fragment from an intracellular protein to present it to a T-cell (cytotoxic T-cell, CD8)

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8
Q

what do class 2 MHCs do

A

hold a peptide fragment from an extracellular protein to present it to a T-cell (helper T-cell, CD4)

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9
Q

which class of MHC works on endogenous antigens, and which class of MHC works on exogenous antigens

A
class 1 works with endogenous antigens
class 2 works with exogenous antigens
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10
Q

what two things can the presentation of endogenous peptides from MHC class 1s tell you about the cell

A
  1. it can show “self” proteins and show that the cell is self
  2. it can show viral proteins and show that the cell has been infected
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11
Q

what does the presentation of exogenous peptides from class 2 MHCs tell you

A

it is only on cells involved in the immune response, and helps target things that shouldn’t be in our systems

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12
Q

From where do you get peptides that class 1 MHC’s present, and who do they specifically present them to?

A

they come from the cytosol and “talk” to Cytotoxic T-cells

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13
Q

from where do you get the peptides that class 2 MHCs present, and who do they specifically present them to>

A

they come from endosomal compartments (exogenous) and are taken from there to the cell surface by MHC class 2s. they “talk” to Helper T-cells

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14
Q

what is the human analog of MHC

A

HLA

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15
Q

what are immature dendritic cells like

A
  • effective phagocytes
  • low class 1 MHC
  • no class 2 MHC
  • recognize cytokines
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16
Q

what are mature dendritic cells like

A
  • less phagocytotic activity

- high MHC levels (both classes)

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17
Q

How do dendritic cells mature

A
  1. on their own (spontaneous maturation)

2. by phagocytosing a microbe

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18
Q

do spontaneously matured dendritic cells activate naive T-cells

A

nope

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19
Q

do activated matured dendritic cells activate naive T-cells

A

yes, maybe the only thing that can do so effectively

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20
Q

how do matured Dendritic cells activate naive-t cells

A
  1. microbes and macrophages cause IL-1 and TNF
  2. IL-1 and TNF cause mature dendritic cells to migrate to secondary lymphoid structures
  3. they express high levels of MHC, B7-1 and B7-2
  4. those interact with CD4 T-cells
    (need the T-cell to bind BOTH the MHC, and the B7s)
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21
Q

what is important in determining compatibility of tissue grafts

A

MHCs

22
Q

what makes dendritic cells hone to secondary lymphoid tissue

A

CCR7

23
Q

what on naive T-cells looks for the B7-1 and B7-2 on activated mature dendritic cells

A

CD28

24
Q

how do the peptide grooves of MHC class 1 and 2 molecules differ

A
class 1  has capped ends and only allows shorter peptides. it also uses one protein as both sides of the binding groove
class 2 doesn't have capped ends and can allow longer peptides. it uses two separate proteins as the sides of the binding groove
25
Q

are all MHC class ones the same

A

no, there are many different class 1 MHCs ( the same for class 2 MHCs) thats why they can cause problems in acceptance of a grafted tissue

26
Q

what is the most gene dense region of the human genome

A

the MHC gene region

27
Q

how are MHC alleles expressed

A

codominantly (both the mom and dads MHCs are expressed)

28
Q

if a human and mouse have three MHC 1 proteins, how many different MHC 1’s can they have on a given cell

A
6
Ad
Am
Dd
Dm
Ld
Lm
d= from dad
m = from mom
29
Q

if a human has three MHC class 2 proteins (a dimer) how many different MHC 2s can they have on a given cell

A

12

30
Q

if a mouse has three MHC class 2 proteins (a dimer) how many different MHC 2s can they have on a given cell

A

8

31
Q

if some species is found to have 4 MHC class 2 proteins (a dimer) how many different MHC 2s could they have on a given cell

A

16
(5 = 20)
(6=24)

32
Q

what do classical MHCs do?

what do non-classical MHCs do

A

classical present peptide antigens to T-cells

non-classical do anything else

33
Q

where do you find the polymorphisms in class 1 and 2 MHCs

A

in the peptide binding grooves

34
Q

what helps the intermediate immune response between innate and adaptive immunity

A

non-classical MHCs

35
Q

what is CD1

A

a non-classical MHC that presents mycobacterial glycolipids to specialized T-cells

36
Q

what enzyme creates the endogenous peptides that are presented by class 1 MHCs

A

proteasomes

37
Q

what is the process of creating peptides that MHC class 1s will present to cytotoxic CD8 t-cells

A
  1. ubiquitin tags the intracellular protein
  2. Proteasomes cleave the peptide in the cytosol
  3. peptidem moves into the ER lumen
  4. it binds to MHC 1 and this creates a vesicle
  5. then it is transferred to the cell membrane
38
Q

what is the difference between constituative proteasomes and immunoproteasomes

A

immunoproteasomes cut peptides into better lengths for MHC class 1s

39
Q

what are DRiPs and how do they relate to MHCs

A

they are defective ribosomal products, and they are usually marked by ubiquitin and cut up by proteasomes, then bound to MHC1 and sent to the membrane

40
Q

what happens to MHC1s that don’t bind a peptide in the ER

A

they are broken down eventually

41
Q

how can viruses counteract their destruction by MHC1s

A

they can stop the process of MHCs binding peptides, and moving to the membrane, so cytotoxic T-cells don’t attack them

42
Q

how does herpes virus prevent being killed by cytotoxic t-cells

A

they stop the MHC 1 from binding peptides and moving to the surface

43
Q

how does the body kill cells that have overcome the MHC1s ability to signal for their destruction

A

NK cells can recognize the low MHC class 1 levels and will destroy the cell

44
Q

what do helper T-cells do once they have been presented the peptide fragment from MHC class 2

A
  1. they show it to macrophages (this activates them to be more efficient killers)
  2. they show it to B-cells (this causes them to differentiate and expand into plasma cells, these create antibodies)
45
Q

how are class 2 MHC’s loaded with peptides

A
  1. MHC 2 in ER is blocked by invariant chain
  2. in a vesicle the invariant chain degrades, leaves CLIP fragement
  3. Exogenous antigen is taken up
  4. HLA-DM switches the antigen and CLIP
  5. it is transported to the membrane
46
Q

what on the T cells helps recognize the MHCs that are presenting peptides to them

A
  1. TCR (T-cell receptor)
  2. either CD8 or CD4
    (if CD8 = cytotoxic T-cell, binds MHC 1)
    (if CD4 = helper T-cell, binds MHC 2)
47
Q

what to TAPS do

A

takes the peptides from the proteasomes and puts them back into the ER, and binds them to the MHC

48
Q

what is cross presentation of exogenous antigens

A

exogenous antigens that are redirected into the enogenous presentation pathway. exogenous peptides with MHC class 1.

49
Q

what cells do cross presentation of exogenous antigens

A

dendritic cells

50
Q

what does cross presentation of exogenous antgens do

A

causes CD8 cytotoxic t-cells to be primed by exogenous antigens (instead of endogenous)