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CBFM Final > Heme Synthesis & Antigen Presentation > Flashcards

Heme Synthesis & Antigen Presentation Flashcards

1
Q

Structure of heme

A

Conjugated double bonds = color
oxygenated = red
deoxygenated = blue

Protoporphyrin IX
Tetrapyyrole ring
4 nitrogen’s
Fe2+ at center

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2
Q

If heme is not associated with protein, its a ____

A

Lipophilic pro-oxidant

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3
Q

Pro-oxidant forms ____

A

ROS - induces oxidative stress

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4
Q

How does lead affect heme synth

A

It inhibits ALA dehydratase and ferrochelatase

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5
Q

Produced in liver when Fe levels are high

Why does it make sense

A

Hepcidin

Because we want to control Fe levels and hepcidin inhibits the transporter ferroportin (the dude on the basolateral side)

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6
Q

What does Hepcidin do

A

Inhibits transport of Fe from the mucosal cell

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7
Q

Inflammatory cytokines increase _______ in the liver, contribute to the ______

A

Synthesis of hepcidin

Anemia of chronic diseases

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8
Q

Where is most heme made

A

Bone marrow and liver

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9
Q

ALAS1 vs ALAS2

A

1: short half life, highly regulated, negative feedback by heme

2: regulated in response to levels of iron

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10
Q

Sideroblastic anemia genetic
What else can cause this is acquired not from genes

A

X-linked mutation of the ALAS2 gene

Most common cause of Sideroblastic anemia
-B6 deficiency also causes this

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11
Q

Sideroblastic anemia acquired

A

Vitamin B6 deficiency
Bad diet
Alcohol abuse

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12
Q

______ are dominantly inherited with low penetrance

A

Genetic porphyrias

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13
Q

Most common porphyrias

A

Porphyria cutanea tarda

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14
Q

_____ has intermittent attacks

A

AIP - acute intermittent porphyria

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15
Q

Where is heme converted to bilirubin

A

Macrophages

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16
Q

Steps of heme to bilirubin

A

Heme—1—->Biliverdin—2—->bilirubin

1=heme oxygenase
need NADPH —>NADP+
need O2
release CO
release Fe3+

2=biliverdin reductase
NADPH —>NADP+

At HOME we first make BILI VERDE (chili verde is harder to make so we need more ingredients) then BILI RUBINS.

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17
Q

Direct vs indirect bilirubin

A

Direct = conjugated, soluble
conjugated by bilirubin glucuronyl transferase
actively transported by MRP2

Indirect = unconjugated, insoluble
carried on albumin to liver

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18
Q

How do you find indirect bilirubin

A

Total -direct

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19
Q

PREHEPATIC jaundice causes

A

Indirect hyperbilirubinemia

If post is directly creepy. This is just the opposite.

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20
Q

What is a common cause of indirect hyperbilirubinemia

A

Over production of bilirubin

From hemolysis = more than one heme being released

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21
Q

INTRAHEPATIC jaundice causes

A

Direct and indirect hyperbilirubinemia

INTRA means inside

If you’re on the inside you’ve got the inside scoop and have both direct and indirect

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22
Q

Mech behind intrahepatic jaundice

A

Something wrong with the liver

It can’t uptake, conjugate and/or secrete bilirubin

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23
Q

How does newborn jaundice happen?

A

Bilirubin glucuronyl transferase is developmentally expressed

This enzyme is low in newborns and even lower in premature newborns

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24
Q

What’s the concern with newborn jaundice

A

Albumin can be at full capacity

This leaves excess bilirubin floating around

It accumulates at the basal ganglia and can cause toxic brain damage called “kernicterus”

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25
Q

How does phototherapy work

A

It converts bilirubin to more soluble isoforms that can be excreated into bile WITHOUT conjugation

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26
Q

What are the genetic conditions causing intrahepatic jaundice

A

Crigler-Najjar Syndrome

Gilbert Syndrome

Dubin Johnson Syndrome

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27
Q

Key points of Craigler-Najjar Syndrome

Type 1
Type 2

A

Rare
Autosomal recessive
Deficiency in bilirubin glucuronyl transferase
Unconjucated hyperbilirubinemia at birth

Type 1 = totally deficient
Type 2 = less severe

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28
Q

Gilbert syndrome key points

A

Common
Mild increase of indirect bilirubin
There is a mutation in the PROMOTER of bilirubin glucuronyl transferase gene

Not very noticeable

GILBERT - GENE
The Gilberts are indirectly creepy

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29
Q

Dubin-Johnson syndrome key points

A

Rare Mutation in MRP2
Causes defective transport of conjugated bilirubin OUT of hepatocytes

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30
Q

Posthepatic jaundice causes

A

Direct hyperbilirubinemia

Post is directly creepy but if you let him be creepy long enough it can lead to indirect

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31
Q

Posthepatic jaundice key points

A

Dark pee
Bile acids can accumulate in plasma
Prolonged obstruction can lead to liver damage and increase of indirect bilirubin

32
Q

Haptoglobin mech/func

A

Hapto:
binds αβ dimers in blood

This creates a complex too big to be filtered by glomerulus

This big boi dimers get delivered to macrophages thru a specific receptor

Then its taken up for release and degradation of heme the normal way

33
Q

Hemopexin mech/func

A

Hemop:
Free Hb is oxidized to metHb

This turns into goblin and
Metheme

Metheme and Hemopexin bing

Takes it to the liver

This action triggers heme oxygenase

34
Q

When does haptoglobin decrease

A

With a lot of hemolysis going on

35
Q

When would haptoglobin increase

A

During inflammation or infection

36
Q

When could hemopexin decrease

A

When there is a lot of hemolysis

37
Q

antigens

A

Molecule or molecular fragment capable of inducing an immune response

38
Q

What are antigens recognized by

A

By specific receptors on T and B cells

39
Q

Immunogen

A

Molecule that stimulate immune response

Antigen focuses more on binding

40
Q

What can be a good immunogen

A

Proteins
Polysaccharides

41
Q

What can be a bad immunogen

A

Nucleic acids - cuz they are inside the cell
Lipids - not water soluble

42
Q

Increasing immunogenicity

A

Worst
amino acids
happens
lipids
steroids
carbohydrates
proteins
Best

43
Q

What are epitopes

A

It’s the part of a macromolecule that the antibody binds to.

Aka determinant

44
Q

What are haptens

A

Small molecule (hapten) attached to large carrier to induce immune response

The hapten carrier complex acts as a immunogen

45
Q

T-dependent antigen process

A

Needs helper T and B lymphocytes to stimulate antibody response

Antigen taken up by dendritic cell

Then the antigen is presented to naive T helper cell

T helper cell interacted with B cell

B cell proliferates

Becomes plasma cell

Secreate antibodies

Example: protein

46
Q

T-independent antigen

A

NON protein antigen that can stimulate antibody response without T cell help

Ex: polysaccharides and lipids

47
Q

Antigen types

A

Metabolites
Sugars
Lipid
Hormones
Macromolecule like complex carbs
Phospholipids
Nucleic acids
Proteins

48
Q

How does T-independent antigen usually work

A

A bunch of epitopes that cross link a bunch of B cell receptors

Directly from there the B cell can proliferate

usually IgM, low affinity antibodies; short-lived plasma cells produced

49
Q

What does Major Histocompatibility Complex do (MHC)

A

Molecule that displays antigen on T cells

50
Q

Inheritance pattern of MHC

A

Codominant expression!

Alleles from both parents are expressed equally amongst children

Typically children won’t have the same inheritance

51
Q

MHC Ι vs MHC II

A

I: present antigen to cytotoxic T cells (CD8)

II: present antigen to T-helper cells (CD4)

52
Q

Cellular expression of Class I MHC

A

6 types
3 independent domains
Stable
If we want to change, we need to mutate
Some are very diverse!
More diversity, more protection against infection

53
Q

Cellular expression of Class II MHC

A

Target extracellular stuff that can’t hide inside cell
they can get microbes that are INTRACELLULAR but they are really good at targeting the extracellular ones
5 isotypes

54
Q

What cells are good at targeting microbes that are INTRACELLULAR

A

NK cells
CD8 T lymphocytes

55
Q

Most polymorphic MHC class I genes

A

HLA locus A, B

56
Q

Most polymorphic MHC class II locus

A

HLA- DRB1

57
Q

Why is it important that there is polymorphism for antigen processing and transplatation?

A

You want the most polymorphic loci to be used because it will have the most likely chance to not be rejected by the new host

The more epitopes there are the more we have a chance of recognizing them

58
Q

Tissue distribution of MHC class I

A

ALL NUCLEATED CELLS IN BODY

59
Q

Tissue distribution of MHC class II:

A

-some activated T cells
-B cells
-macrophages/APC
-thymic epithelial cells

60
Q

Big function of NK cells

A

Kill cells that don’t have MHC I

61
Q

Which MHC has 2 anchors

A

MHC I

62
Q

One anchor domain allows for what

A

Longer peptide to dangle out
MHC II

63
Q

Exogenous antigen presentation via MHC class II

A
  1. Endocytos protein (with antigen) into cell
  2. Process protein in endosome and lysosome
    break it down
  3. At same time in RER
    a. ER is making MHC II with CLIP and friends (invariant chain) (CLIP is just a dude filling the hole. His friends make sure no one else fills the hole)
    b. MHC II with CLIP goes to golgi
    c. From golgi, it is now in a exocytic vesicle
    here CLIPS friends leave
  4. Exocytic vesicle with MHC II and CLIP combine with endosome/lysosome that has antigen
  5. NOW antigen and MHC II are in the same place
    as well as HLA-DM
    function of this is to accept CLIP does this by catalyses
  6. Antigen fills in hole at MHC II spot
  7. It is presented on the outside of the cell
64
Q

Exogenous vs endogenous antigen presentation basics

A

EXO: antigen presented and created outside cell

ENDO: antigen presented and created inside cell

65
Q

MHC II do what kind of presentation of antigen

A

Exogenous

66
Q

____ is only in antigen presenting cells

A

Exogenous presentation

67
Q

MHC I do what kind of antigen presentation

A

Endogenous

68
Q

Endogenous antigen processing is used for processing ______

A

Cytosolic proteins

69
Q

Endogenous proteins include

A

Viral gene products
Proteins from phagocytoses microbes
Mutated/altered host cell genes

70
Q

Endogenous peptide processing steps

A
  1. Production of proteins in CYTOSOL
  2. Transported to proteasome
  3. Breaks down protein to peptides
  4. Peptides transported to ER by TAP transporter
  5. At the same time MHC I and β2m transported to ER
    here they form weak connection with TAP and other chaperone molecules
    6.Tapsasin forms bridge btw MHC I and TAP
    this allows the peptide to enter the peptide binding cleft of MHC I
  6. MHC I gets folded properly and is exported to cell surface
71
Q

Describe cross presentation

A

APC can take in either exogenous or endogenous and load it to MHC I

72
Q

Benefit of cross-presentation

A

Don’t want APC to get infected
this would effect T cells in the long run

73
Q

Process of cross presentation

A

1.Transfer of antigen from Endocytic pathway to cytosol
2. Picked up by proteosome
3. Processed
4. Transported to ER for presentation on class I MHC

74
Q

Endogenous antigen processing includes

A

Viral gene products
Proteins from phagocytoses microbes
Mutated/altered host cell genes

75
Q

Define porphyria

A

Abnormal build up of heme sythesis intermediates

76
Q

What is the goal of having haptoglobin and Hemopexin?

A

They salvage proteins Hb fragments from intravascular hemolysis

(Put in own words)

77
Q

Where is ALAS1

A

Liver, and other tissues

CBFM Final (18 decks)

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