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CBFM Final > Heme Synthesis & Antigen Presentation > Flashcards

Heme Synthesis & Antigen Presentation Flashcards

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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
How does phototherapy work
It converts bilirubin to more soluble isoforms that can be excreated into bile WITHOUT conjugation
26
What are the genetic conditions causing intrahepatic jaundice
Crigler-Najjar Syndrome Gilbert Syndrome Dubin Johnson Syndrome
27
Key points of Craigler-Najjar Syndrome Type 1 Type 2
Rare Autosomal recessive Deficiency in bilirubin glucuronyl transferase Unconjucated hyperbilirubinemia at birth Type 1 = totally deficient Type 2 = less severe
28
Gilbert syndrome key points
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
29
Dubin-Johnson syndrome key points
Rare Mutation in MRP2 Causes defective transport of conjugated bilirubin OUT of hepatocytes
30
Posthepatic jaundice causes
Direct hyperbilirubinemia Post is directly creepy but if you let him be creepy long enough it can lead to indirect
31
Posthepatic jaundice key points
Dark pee Bile acids can accumulate in plasma Prolonged obstruction can lead to liver damage and increase of indirect bilirubin
32
Haptoglobin mech/func
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
Hemopexin mech/func
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
When does haptoglobin decrease
With a lot of hemolysis going on
35
When would haptoglobin increase
During inflammation or infection
36
When could hemopexin decrease
When there is a lot of hemolysis
37
antigens
Molecule or molecular fragment capable of inducing an immune response
38
What are antigens recognized by
By specific receptors on T and B cells
39
Immunogen
Molecule that stimulate immune response Antigen focuses more on binding
40
What can be a good immunogen
Proteins Polysaccharides
41
What can be a bad immunogen
Nucleic acids - cuz they are inside the cell Lipids - not water soluble
42
Increasing immunogenicity
Worst amino acids happens lipids steroids carbohydrates proteins Best
43
What are epitopes
It’s the part of a macromolecule that the antibody binds to. Aka determinant
44
What are haptens
Small molecule (hapten) attached to large carrier to induce immune response The hapten carrier complex acts as a immunogen
45
T-dependent antigen process
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
T-independent antigen
NON protein antigen that can stimulate antibody response without T cell help Ex: polysaccharides and lipids
47
Antigen types
Metabolites Sugars Lipid Hormones Macromolecule like complex carbs Phospholipids Nucleic acids Proteins
48
How does T-independent antigen usually work
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
What does Major Histocompatibility Complex do (MHC)
Molecule that displays antigen on T cells
50
Inheritance pattern of MHC
Codominant expression! Alleles from both parents are expressed equally amongst children Typically children won’t have the same inheritance
51
MHC Ι vs MHC II
I: present antigen to cytotoxic T cells (CD8) II: present antigen to T-helper cells (CD4)
52
Cellular expression of Class I MHC
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
Cellular expression of Class II MHC
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
What cells are good at targeting microbes that are INTRACELLULAR
NK cells CD8 T lymphocytes
55
Most polymorphic MHC class I genes
HLA locus A, B
56
Most polymorphic MHC class II locus
HLA- DRB1
57
Why is it important that there is polymorphism for antigen processing and transplatation?
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
Tissue distribution of MHC class I
ALL NUCLEATED CELLS IN BODY
59
Tissue distribution of MHC class II:
-some activated T cells -B cells -macrophages/APC -thymic epithelial cells
60
Big function of NK cells
Kill cells that don’t have MHC I
61
Which MHC has 2 anchors
MHC I
62
One anchor domain allows for what
Longer peptide to dangle out MHC II
63
Exogenous antigen presentation via MHC class II
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
Exogenous vs endogenous antigen presentation basics
EXO: antigen presented and created outside cell ENDO: antigen presented and created inside cell
65
MHC II do what kind of presentation of antigen
Exogenous
66
____ is only in antigen presenting cells
Exogenous presentation
67
MHC I do what kind of antigen presentation
Endogenous
68
Endogenous antigen processing is used for processing ______
Cytosolic proteins
69
Endogenous proteins include
Viral gene products Proteins from phagocytoses microbes Mutated/altered host cell genes
70
Endogenous peptide processing steps
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 7. MHC I gets folded properly and is exported to cell surface
71
Describe cross presentation
APC can take in either exogenous or endogenous and load it to MHC I
72
Benefit of cross-presentation
Don’t want APC to get infected this would effect T cells in the long run
73
Process of cross presentation
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
Endogenous antigen processing includes
Viral gene products Proteins from phagocytoses microbes Mutated/altered host cell genes
75
Define porphyria
Abnormal build up of heme sythesis intermediates
76
What is the goal of having haptoglobin and Hemopexin?
They salvage proteins Hb fragments from intravascular hemolysis (Put in own words)
77
Where is ALAS1
Liver, and other tissues

CBFM Final (18 decks)

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