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immunology 2 Flashcards

1
Q

in basic terms what is a MHC and function?

A

they will be bound to an antigen and they bind to t cells which then undergo clonal expansion and differentiation into active t cell.

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2
Q

how do dendritic cells carry an antigen to the lymph nodes and back to the infected tissue? (4 steps)

A

EPITHELIUM: Dendritic Cells use PRR to find PAMPs and macrophages cut up the pathogen and recruit help through cytokines. Dendritic cells take the antigen.
LOCAL INFECTION: Cytokines make dendritic cells move to lymph nodes. Dendritic cells now differentiate into mature dendritic cells that help stimulate naive t cells.
LYMPH NODE: Mature dendritic cells original home to T cell area and present an antigen there. Naive T cells under clonal expansion and develop effector function.
Effector CD4 ThCells activate B cells.
BACK TO INFECTED SITE: Effector CD8 Tc cells will kill target cells. Effector Cd4 Th activate macrophages. PAMP cut up the pathogen and present on MHC to show T cell. Adaptive immune response helps innate response

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3
Q

how do dendritic cells present pathogen to naive t cells?

A
  1. Antigen-loaded dendritic cells show peptides from pathogen using MHC
  2. Naive t cell scans the surface of antigen and dendritic cells to see if TCR recognizes the peptide. (MHC surface of cell)
  3. Dendritic cells activates pathogen specific naive t cell to become effector cell.
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4
Q

where are dendritic cells mostly found?

A

throughout the body (ubiquitous)

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5
Q

what is the mechanism of antigen uptake for dendritic cells?

A

They do it by macopinocytosis and phagocytosis via PRRs and viral infection

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6
Q

What is the MHC II expression for dendritic cells?

A

Constitutive on immature dendritic cells.
increases with interferon gamma and increases inflammation.
high on dendritic cells in lymphoid tissues

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7
Q

what about co-stimulators on dendritic cells?

A

Constitutive on immature dendritic cells. Increases with interferon gamma and high on mature dendritic cells in lymphoid tissue.

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8
Q

what is the main function of dendritic cells?

A

they present antigens to naive T cells and they start the primary immune responses like clonal and effector.

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9
Q

where are macrophages found?

A

connective tissue, body cavity, lymphoid tissue

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10
Q

how do macrophages take in antigens?

A

phagocytosis via PRRs

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11
Q

what is the MHC II expression for macrophages?

A

low and negative inducible by interferon gamma

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12
Q

what about co-stimulators of macrophages?

A

low and inducible by PRR ligation and interferon gamma and interaction with T cells.

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13
Q

what is the main function of macrophages?

A

Do antigen presentation to CD4 effector T cells and they promote cell-mediated immunity

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14
Q

Where are the B cells found?

A

lymphoid tissue

peripheral blood

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15
Q

how do B Cells take in antigens?

A

They take it in through their B cell recptor (BCR)

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16
Q

What is the MHC II expression for B Cells?

A

Constitutive and increases with cytokines (IL-4)

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17
Q

what about the co-stimulators of B cells?

A

Induced by BCR X-linking and interaction with T cells.

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18
Q

What is the main function of B cells?

A

Antigen presentation to CD4 helper t cells.

promote humoral mediated immunity

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19
Q

what is the benefit of polygeny and polymorphism in terms of MHC gene recombinations?

A

increase in polymorphism, increase in polygeny means that there is an increase in potential polypeptide-binding motifs to show to T cells.

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20
Q

What are the HLA genes associated with MHC I?

A

HLA, HLB, HLC

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21
Q

what type of T cells are associated with MHC I and are the antigens endogenous or exogenous?

A

CD8 or cycotoxic T cells are associated.

The toxins are inside the infected host so they are endogenous.

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22
Q

what makes up the binding groove of the MHC I?

How does it help present antigens?

A

They have an alpha and beta subunit.
They anchor the peptides and it does not hang out of the groove. The peptide has an anchor amino acid and it helps interact with the MHC.

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23
Q

What are the steps of preparation and presentation for MHC I?

A
  1. Endogenous Antigen is cleaved by a PROTEASOME (chopped up, and tagged with ubiquitin).
  2. Transported to the ER by TAP.
  3. Peptides breakaway from TAP and bind to MHC and beta-2-microglobulin (chaperone help this)–TAPASIN
  4. Peptide MHC I complex (MHC+Antigen) goes to the golgi.
  5. From golgi to the surface to present to CD8 (cytotoxic T cell).
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24
Q

What are the HLC genes associated with MHC II?

A

DP, DQ,DR, DRp

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25
Q

what type of T cells are associated with MHC II and are the antigens endogenous or exogenous?

A

CD4 or Helper T Cells are associated.

The toxins are from the outside so they are exogenous.

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26
Q

What makes up the binding groove of MHC II?

How does it help present antigens?

A

Alpha and beta subunit.
peptide is presented and it is much longer than a peptide needed for MHC I.
anchor residue is distributed along the length of the peptide and the amino acids bind to the MHC.

27
Q

what are the steps of preparation and presentation for MHCII?

A

Two processes will be going on almost at the same time.
1. Exogenous antigen will enter the cell through vesicles (endocytosis, phagocytosis)
2. Exogenous antigen is degraded (broken up) by lysosomal endosomal proteases (cathepsins) –late endosome.
A. Alpha and beta chain made in ER make the complex and it has a membrane bound invariant chain (li) bound to it in order to stop MHC from binding peptides)
B. Li facilitates transport of the vesicles with MHC II across the golgi.
C. Directs MHC II to late endosome
3. Proteolytic degradation of the Li in the MHC II leaves behind CLIP(degrades invariant chain and protects MHC peptide binding groove from binding)–ANTIGEN AND MHC NOT BOUND YET!!!
4. HLA-DM removes CLIP and loads peptides.
5. Peptide-MHC II complex is transported to surface for presentation to CD4 T cell.

28
Q

what happens after presentation of antigens for MHC I?

A

After presentation the cytotoxic T cell will kill the antigen-expression infected cell.

29
Q

what happens after presentation of antigens for MHCII?

A

The CD4 helper T cell will release cytokines that will cause macrophages to destroy the phagocytosed microbe and B cell antibody secretion.

30
Q

Describe the B Cell Receptor

A

Will take an antigen of any form
no transmembrane receptor for antibodies
2 binding sites
heavy and light arms that are identical for 2 identical antigen binding sites per receptor molecule.
stabilized by multiple chemical bonds and has potential for bivalent interaction that is strong.

31
Q

Describe the T Cell Receptor?

A 
alpha and beta chain
need to bind to MHC.
loaded will give information for T cell.
MHC is stabilized by CD4 and CD8
Receptor antigen contacts are minimal and receptor MHC dominant works better for weak affinity.
One binding site.
32
Q

will we show all possible recombinations at once?

A

No, we will only show a few during our lifetime.

33
Q

Describe the steps of T-Cell development.

Where does the receptor come into play?

A
  1. T cell originates from a stem cell in the bone marrow and. No receptor.
  2. Through the use of interleukin 7 the stem cell now becomes a Pro-T cell and is now in the bone marrow.
  3. The Pro-T will progress into Pre-T. Has a recombined beta chain. Now showing Pre-T receptor.
  4. Through interleukin 7 Pre-T will progress into double positive. The Membrane TCR will now be there. (Double positive not differentiated into CD4 or CD8 just yet.
  5. From double positive it moves into a Single Positive (immature T cell). It is still in the thymus and is now either a CD8 or CD4 T cell.
  6. Once the single positive leaves the thymus to go into the periphery it becomes a naive mature T-cell. It has a TCR and can be involved in proliferation and differentiation.
34
Q

How many checkpoints are there in T cell development?

A

There are three checkpoints.

35
Q

describe checkpoint 1 of T cell development.

A

It is between the Pre-T receptor to make sure the membrane assembled beta chain occurred. In order to survive it needs to have: successfully rearranged Beta chain, associated with PT-beta, association with CD3+zeta, and express both CD4 and CD8.
*allelic exclusion

36
Q

What is allelic exclusion?

A

only one gene is one

each lymphocyte has one specificity

37
Q

Describe checkpoint 2.

A

In order to survive it has to have the capacity of the TCR to interact with MHC+Peptide.
The peptide is self-made and it will bind to the MHC and then to the TCR and this will help with differentiation.
If the self-made peptide is a CD4 then it will make a CD4 cell and vice versa for CD8.
If it does not bind to self-MHC then it will undergo apoptosis.

38
Q

What is central tolerance?

A

It is self tolerance that is established during t cell development in the thymus and it ensures that it will not be autoreactive to self.

39
Q

Describe checkpoint 3.

A

Central tolerance.
Some cells will have a higher threshold for activation–more selection for receptor.
Positive and negative selection.
high affinity for binding to self=negative selection–death
low affinity for binding to self=positive selection–go to the periphery.

40
Q

Describe the steps of B cell development.

A
  1. Stem cell in the bone marrow.
  2. interleukin 7 helps it turn into Pro-B and is still in the bone marrow. no receptor yet.
  3. Pro-B to Pre-B. still in the bone marrow. Pre-B receptor now.
  4. Will have to undergo light chain rearrangement in order to progress into an immature B cell. Now sent out into the periphery.
  5. The immature B cell will now progress into a mature B cell. VDJ recombination could still occur. Membrane Immunoglobulin M and D. Now in the periphery and can now undergo activation (proliferation and differentiation)
41
Q

describe the checkpoint for B cell development.

A

Check to see if the B Cell Receptor structure is functioning. In order to survive the H chain has to be rearranged and it has to have an associated light chain. Immunoglobulin signaling molecules have to be there.
The results are that proliferation could happen, allelic exclusion (stop Heavy chain recombination), and start and stimulate L chain recombination

42
Q

what are the two things that must happen for cell-mediated immunity to occur?

A
  1. Antigen on the MHC on the APC binds to the T cell Receptor
  2. Co-Stimulation: CD28 binds to B7 (T cell to APC)
43
Q

what is an immune synapse?

A

It is the antigen binding to the t cell receptor and CD28 binding to B7 and the presence of CD4.

44
Q

How do T cells differentiate into different types of T helper cells?

A

Generally, the APC releases cytokines that are specific to the pathogen. Help tailor the immune response to the pathogen.

45
Q

the activated t helper cell will down or up regulate IL-2?

what is the purpose?

A

It will up regulate IL-2 more specifically the alpha receptor.
IL-2 and t helper cells will bind and cause clonal expansion to itself. (autocrine signaling)

46
Q

How do TH1 cells come to be?

A
  1. Occurs when macrophages, bacterially infected cells, and dendritic cells make IL-12. Natural Killer cells will make interferon gamma. Virally infected cells makes interferon alpha, beta, and gamma.
  2. Many of the cytokines will bind to the T cell and make it make transcription factors that cause genes to express TH1 genes.
  3. TH1 cells secrete interferon gamma that reinforces the process.
47
Q

What do TH1 cells do?

A
  1. They secrete interferon gamma that boosts the macrophages ability to kill injested pathogens by increase ROS, NO, and lysosomal proteases.
  2. Express CD40 ligand on cell surface and bind to CD40 on macrophages that stimulate them.
  3. Express IL-12 which make Natural killer cells more effective.
  4. Also produce IL2 which makes natural killer cells, CD8, and B cells proliferate.
48
Q

What happens when TH1 is not carefully controlled?

A

autoimmune.

49
Q

How do TH2 cells come to be?

A
  1. Occurs when a worm too large gets destroyed by eosinophils, basophils, and mast cells , which dump their toxic granules full of protesase and hydrolyases. Kills parasite.
  2. macrophages and dendritic cells will pick up the left overs. These presents IL4,5, 10 in the immune symapse.
  3. These cytokines will bind to the T cell which cause the T cell to release transcription factors that transform it into a TH2 cells.
50
Q

what is the purpose of TH2 cells?

A
  1. Produces cytokines IL4,5,10,13 and stimulate B cells to make IgE to coat the worms.
  2. Stimulate mast cells, basophils, eosinophils to bind FC regions of IgE to degranulate and kill the parasite.
  3. IL13 stimulates mucosal secretion and intestinal peristalsis to help get the worm out.
  4. IL4,5 help stimulate TH2 cells themselves to reinforce the process.
51
Q

what happens if no work and are still used?

A

asthma and allergies

52
Q

How do the TH17 come to be?

A
  1. Extracellular bacteria and fungi are picked up by macrophages and dendritic cells.
  2. APCs make IL1,6,23,TGF-beta in the immune synapse.
  3. These cytokines will bind to the T cell and cause it to make transcription factors that cause genes to get expressed in the T cell transforming it into a TH17 cell.
53
Q

What is the purpose of TH17 cells?

A
  1. Produce IL17 that recruits neutrophils that engulf extracellular pathogens and destroys them.
54
Q

what happens if TH17 is uncontrolled?

A

asthma and autoimmune.

55
Q

How do T follicular helper cells come to be?

A

They live in the follicle of lymph nodes and their role is to help generate memory B cells.
1. occassionally APC will make IL6,7,27 and these cytokines will be released and bind to the T cell to make transcription factors that cause a number of genes to get expressed that transform the T cell to turn into a TfH cell.

56
Q

What is the purpose of TfH cells?

A
  1. Produce CD40 on the cell surface and binds to the CD40 receptor on B cells and makes them express cytokine receptors.
  2. IL21 and interferon gamma produced will stimulate B cells to make IgG antibodies and become memory B cells.
57
Q

For CD8 cells do they need to directly interact with antigen? Intracellular antigen or extracellular antigen?

A

Yes they need to react directly to the antigen. Intracellular antigen.

58
Q

Do CD8 cells need to have a decrease in stimulation to become activated?

A

No they need an increase in stimulation. (cross-presentation)

59
Q

How do CD8 work?

A
  1. Will keep randomly binding until it binds to the right one.
  2. LFA1 binds tightly to ICAM on antigen.
  3. will form SMAC after tightening because of a change in the cytoskeleton.
  4. Will then release granules that punch holes and activate caspases which causes the target cell to undergo apoptosis.
  5. It will pop off once job is done and will go and kill another cell that could be infected.
60
Q

why is IL-2 important and what is the primary cell source?

*adaptive

A

it is a cytokine secreted by T cells that help with their proliferation. it also increases cytokine synthesis and potentiates Fas-mediated apoptosis. it also helps NK and B cells proliferate and NK will become active

61
Q

why is IL-4 important what is the primary cell source?

*adaptive

A

it is a cytokine secreted by CD4 (TH2) cells and mast cells.
B cells: helps with isotype switching to IgE
T Cells: helps with TH2 differentiation and proliferation.
Macrophages: inhibition of interferon gamma mediated activation
Mast cells: proliferation

62
Q

why is interferon gamma important and what is the primary cell source?
*adaptive

A 
T cells (TH1 and CD8 cells) and NK cells are sources
Macrophages: activation (increased microbicidal functions)
B cells: isotype switching to opsonizing and complement fixing IgG
T cells: TH1 differentiation
63
Q

why is IL-17 important and what is the primary cell source?

*adaptive

A

T cells are the primary cell source.
Endothelial cells: increased chemokine production
macrophages: increased chemokine and cytokine production
T cells: T cell differentiation

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