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IHO Week 4 > Diebel- Antigen presentation and processing > Flashcards

Diebel- Antigen presentation and processing Flashcards

1
Q

Describe the life of a cell in the immune system….

A

Differentiation:
Immature > mature >

Activation/Induction:
Resting > Activated (Effector) > Memory > activated

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2
Q

What is anergy?

A

Anergy is a way to weed out cells and prevent auto-immunity. It occurs when a T cell binds self antigen w/ out co-stimulatory molecule present (B7)

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3
Q

What do you need for full T cell activation?

A

Dual signaling!

The act of the APC ingesting antigen and breaking it down stimulates the expression of B7. Dual signaling required proper Tcr and co-stimulatory interarctions.

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4
Q

What is CTLA-4?

A

Regulates T cell response over a fixed period of time

T cell presented CD28 eventually turns into CTLA4 which still binds to APC but inhibits it. This ensures that the cell only performs it’s functions for 3-4 days.

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5
Q

Most cells in the body present both ___________using _________which is recognized by _______.

A

Foreign and self antigens
MHC I
CD 8 killer T

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6
Q

Professional APCs also present antigens using ______ which is recognized by___________.

A

MHCII

CD 4 helper T

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7
Q

Which is the most effective APC?

A

Dendritic cells

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8
Q

B7 is equivalent to what CD?

A

CD80/86

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9
Q

Immature Dendritic Cells

MHCII expression?
B7 C0-stimulation expression?

A

both are constitutively expressed at low levels

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10
Q

Mature dendritic cells

MHCII expression?
B7 C0-stimulation expression?

A

Both are constitutively expressed at high levels

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11
Q

Macrophages

MHCII expression?
B7 C0-stimulation expression?

A

MHCII- must be activated by phagocytosis to express

B7- must be activated to express

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12
Q

B cells

A

MHCII- constitutively expressed (increases w/ activation)

B7- must be activated to express

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13
Q

Compare the cytosolic and endocytic pathway.

A

Cytosolic:
intracellular protein synthesis of endogenous antigen–>RER–>MHCI–> surface

Endocytic:
MCHII made in RER–> cell takes up exogenous antigen from environment–> put on MHCII–> surface

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14
Q

Proteins in the cell are degraded by ______. What are it’s components?

A

Proteasomes!

20S component- active part involved in breaking down the protein into bits

19S lid-recognizes and binds ubiquitin

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15
Q

What is ubiquitin?

A

Tags things like viruses to be bound to 19s regulator and thrown away in the proteasome trash can.

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16
Q

What triggers a proteasome to switch out it’s components and become an immunoproteasome? Why is this impt?

A

TNFa

IP is more efficient at degrading protein to the right size/charge to load onto MHC complexes.

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17
Q

What happens when IP is present (i know this is redundant…)?

A

You break down proteins and load them onto MHCI MUCH BETTER than a constitutively active proteasome.

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18
Q

What is TAP?

A

transporter associated with antigen processing

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19
Q

What does TAP do?

A

TAP proteins extend across the RER membrane and transport cytosolic peptides into the lumen of the RER where peptides are being loaded onto Class I molecules.

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20
Q

Tap complex has an affinity for peptides of _______ amino acids. What is the optimal binding size? Who does the final trimming of biggies?

A

8-16 AA
9 AA

ERAAP

21
Q

Describe the process of peptide loading onto MHC I.

A
  1. Synthesis and embedding of alpha chain of MCHI into cell surface.
  2. Calnexin binds and stabilizes protein so it can obtain proper 3D shape.
  3. Calnexin lets go.
  4. B2 binds.
  5. Peptides are broken down in proteasome. If they’re the proper length they get through TAP I/II complex.
  6. TPS is a mediator to ensure that MCH I is right next to the TAP complex.
  7. If peptide is bigger than 9 aa long, ERAAP acts on the peptide prior to loading.
  8. One MCHI and peptide are bound, complex moves from RER to the cell surface
22
Q

What are DRiPS and what happens to them? What cuases them?

A

Proteins that are synthesized incorrectly. They are rapidly degraded and presented on the cell surface w/ MCH I.

*UV radaiton–> mut DNA–> aberrant proteins

DRiPs signal IS to kill cells that are defective

23
Q

Virus infected cells contain a distinct 20S proteasome that is induced by_______ and works to________

A

IFNy and TNFa
Degrade and present viral proteins on the cell surface thorugh MCHI

**allows for recognition and killing of cells infected w/ viruses

24
Q

How do T cells interactions w/ MHC I eventually lead to cell death.

A
  1. Two instructional signals (activated)
  2. Recognize antigen on MCH I
  3. Release cytotoxic molecules (IFNy and TNFa)
  4. Bind to death receptor and release perforin–> apoptosis
  5. Granulysis pokes holes in target cell membranes —> apoptosis.
25
Q

Where do you find Class I and Class II genes? Where is B2 microglobulin?

A

chromosome 6

chromosome 15

26
Q

How do we know that kids w/ MCHI def can still fight some viral infections?

A

Though they have a profound def in CD8 T cells, and a decreased ability to present antigens to CD8 T cells they still….

Have INCREASED levels of IgG (B cells can diff)

They have specific Ab to certain infections.

27
Q

What happens clinically to kids w/ MCH I def?

A

Viral infections damage their airway and leave them more susceptible to bacterial infections.

28
Q

Why is a reduction in CD8 T cells a direct result of lack of MCH I class production?

A

Lymphocytes NEED to interact w/ MCH clas I molecules in order to mature. (This is where positive selection happens).

29
Q

Why do people w/ MCH I def have delayed type hypersensitivity?

A

Because they still have CD4 T cells.

30
Q

Why do people w/ MCH I def have overactive NK cells? What does this cause?

A

Any hint that a cell is in trouble causes a NK cell to bind especially b/c it perceives that there isn’t as much MCH I as there should be. If you’re not displaying MCH I, then NK will be more likely to kill any cell that throws out a stress signal.

This can lead to granulatomatous lesions.

31
Q

How are antigens internalized into APCs in the endocytic pathway? DC, Macro, B cell?

A

Exogneous antigens are internalized via endocytosis or phagocytosis.

DC/Macropahges- phagocytize
B cells- receptor mediated endocytosis

32
Q

Where are internalized antigens degraded in the endocytic pathway?

A

phagolysosomes or endosomes

33
Q

What are the 2 ways that macrophages and DCs can internalize antigens?

A
  1. Phagocytosis

2. TLRs through receptor mediated endocytosis

34
Q

Describe the assembly of a MCH II molecule.

A
  1. Make alpha and beta chains of class II.
  2. Block the alpha and beta chain w/ an invariant chain (CD74)
  3. The invariant chain degrades over time and turns into a clip.
35
Q

What does a clip do?

A

A clip blocks a binding site until a peptide is present or until another molecule removes the clip and allows for binding.

36
Q

What are the roles of the invariant chain?

A
  1. assist w/ folding of class II alpha and beta chains
  2. Bind to peptide-presenting site of Class II molecule and assist in transport of MHCII from golgi to cytoplasmic vesicles
37
Q

What catalyzes the exchange of the antigenic peptide for the CLIP?

A

HLA-DM (which can be regulated by HLA-DO)

38
Q

What does HLA-DO do and where is it expressed?

A

B cells and in the thymus

It blocks HLA-DM in very acidic conditions (late endosome)

39
Q

What do HLA-DO and HLA-DM do?

A

Ensure that the peptide is being loaded at the appropriate point in proteasome degradation.

40
Q

What is cross presentation?

A

DC first must license the Th to become functional. Then the T cell feeds back instructions (cytokines) to the DC to activate class I.

41
Q

What is a MHC II deficiency?

A

A failure of gene regulation

42
Q

MCH Class II is inherited as what type of trait?

A

Autosomal recessive

43
Q

In someone born with an MCH II def, when do health problems show up? how do these problems present?

A

Early in infancy

Mild form of combined immunodeficiency–increased suceptibility to pyogenic and opportunitistic invecionts

44
Q

How do infants w/ MCH class II def differ from infants w/ SCID?

A

They have T cells which can respond to nonspecific T T cell mitogens like PHA

45
Q

What is the diff between MCH class I and II def?

A

MCHII- deficient in CD4 T cells, mod to severe hypogammaglobulinemia

MCH I- CD8 T are very low, CD4 T are normal

46
Q

What is the treatment of choice for individuals w/ MCH II def?

A

Hematopoietic stem cell transplant

47
Q

Why is a hematopoietic stem cell transplant not a good treatment for class I?

A

Every cell that makes MCHII comes from the hematopoietic stem cell population. So you replace the precursor population and you get MCH II up and running.

Whereas all nucleated cells express MCH I–it’s impossible to transplant a WHOLE PERSON!

48
Q

What is the role if INF-y in MCH II def?

A

INF-y usually induces the expression of MCH II molecules on APC, but it FAILS to induce expresson on APCs of pts w/ MCH II def.

**suggest that the defect might be in the regulation of expression of MCH II genes.

49
Q

The defect in MCH II def is related defects in the regulation of gene expression and specifically…

A

Transcription factors.

IHO Week 4 (15 decks)

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