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HDM - Midterm > CIS - Bowden > Flashcards

CIS - Bowden Flashcards

1
Q

What is HERD immunity? 8

A

People that are vaccinated (Ag-immunized) protect individuals who aren’t by lowering the exposure of Ag

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2
Q

What are two examples of passive immunization? 10

A

Snake bite antivenom

Passive transfer of Ig from mother to child

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3
Q

What are two examples of active immunization? 11

A

Natural exposure to pathogens

Vaccines

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4
Q

Which immunization is immediate and which is delayed? 10

A

Active immunization –> delayed

Passive immunization –> immediate

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5
Q

What is the function of passive-active immunizations? What an example? 12

A

Gives both an immediate, but also an active, delayed (and therefore memory) protection

Ex.
Tetanus
Rabies

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6
Q

Is IgM produced after birth? 14

A

No, IgM is produced while still a fetus (the first Ig to be produced by fetus)

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7
Q

What are types of live vaccines? 17

A

Live viruses from different species

Live, attenuated viruses

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8
Q

What are example of inactivated vaccines? 17

A

Killed/inactivated viruses

Toxoid

Conjugate

Subunit or component of virus

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9
Q

What are two experimental vaccines? 17

A

DNA

Recombinant vector

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10
Q

How can a vaccine be produced against haptens? 21

A

Through development of conjugated vaccines

Link a polysaccharide to the antigen to form an immunogen (Ag is a hapten in this case)

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11
Q

What’s the difference between the “a” and “b” fragments of complement? 35

A

“a” fragment is smaller (anaphylatoxins)

“b” fragment is larger and usually binds the target

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12
Q

What happens in the classical pathway? 40, 41, 42, 43

A

IgM or IgG Ab becomes bound to Ag

Next, C1 component binds Fc region of Ab

C1 releases C1r and C1s forms a C1qrs complex

C1qrs complex cleaves C4–> C4a + C4b

C4b attaches to bacterial cell membrane

C4b-bacteria complex attracts C2

Once C2 enter area C1qrs cleaves it, C2–> C2a + C2b

C2a stays with C4b-bacteria complex make a complex called a C3 Convertase C3 –> C3a + C3b

C3b joins C4b-C2a-bacteria to form C5 Convertase (C4b2a3b)

C5 –> C5a + C5b, C5b initiates MAC formation

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13
Q

How does the classical pathway amplify itself (minor)? 42

A

C1qrs continuously cleaves C4

(C4b attaches to bacterial membrane and forms a three-part complex with C2a)

C4b2a is our C3 convertase!

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14
Q

Why is C3 such a good opsonizer? 43

A

C3b is unable to bind self-surfaces, but deposits quickly on non-self surfaces

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15
Q

What is the major way in which the classical pathway activates itself? 43

A

C3 convertase cleavage of many C3

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16
Q

What is the composition of C5 Convertase? 43

A

C4b2a3b

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17
Q

What forms the MAC? 44

A

C5b, C6, C7, C8, C9

First, C5b67 inserts (7 actually in membrane)

C8 associates and attracts C9

C9 forms the pore (10 - 16 copies)

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18
Q

Recite a walk through of the alternative pathway? 46, 47

A

C3 spontaneously and constantly converts to C3b and C3a

C3b further auto cleaves to iC3b aka Factor I

C3b lands on bacteria and marks the bacteria

Factor B in the area sees C3b and latches on

Factor D sees the relationship and cleaves Factor B –> Ba + Bb

Bb stays attached to C3b forming a C3 convertase (C3bBb) = amplification

With the amplification more C3b is produced

Eventually, another molecule of C3b joins the C3 Convertase (C3bBb) –> C3bBb3b forming a C5 Convertase

C5 Convertase –> C5a + C5b

C5b initiates MAC formation

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19
Q

Why does C3b not bind self-surfaces? 46

A

Sialic acid on self-surfaces rapidly inactivates C3b

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20
Q

What extends the life of C3bBb and C3bBb3b complexes on bacteria? What the hell are these complexes? 48

A

C3bBb –> C3 Convertase (alternative pathway)

C3bBb3b –> C5 Convertase (alternative pathway)

Properdin extends the half-life of both of these convertases

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21
Q

At what point do the alternative and classical pathway merge? 48

A

With the formation of MAC

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22
Q

Where is mannose-binding lectin found and what is it? 50

A

Found in the plasma

From the collectin family, a typeof Ficolin

23
Q

What cleaves mannose-binding lectin? 50

A

MBL cleaved by MASPs

MBL-associated serine proteases

24
Q

Recite a walk through of the Lectin Pathway? 51

A

MBL (mannose binding lectin) binds mannose residues of a bacterium and activates MASP 1/2

Activated MASP 1/2 becomes a C2 and C4 convertase

C2 –> C2a + C2b | C4 –> C4a + C4b

C4b-C2a-Bacterium = C3 Convertase: C3 –> C3a + C3b

C3b-C4b-C2a-Bacterium = C5 Convertase: C5 –> C5a + C5b

25
Q

In addition to deficiency of C3 what else can mimic C3b exhaustion? 53

A

Lack of regulators Factor H and Factor I results in overproduction of C3b leading to its exhaustion from the serum

26
Q

With a MAC deficiency, what two infections would you expect to see occur more often? 54

A

Neisseria gonorrhoeae

N. Meningitidis

27
Q

What is the most commonly identified form of complement deficiency? 54

A

C2 deficiency

28
Q

What disease is caused by C2 deficiency and why? 54

A

Systemic lupus erythematosis (SLE)

Immune complexes build in blood vessel walls –> activates complement –> inflammation –> promotes breakdown of self-Ag tolerance

29
Q

What are the two ways in which regulators of complement activation regulate? 55

A

Binding with dissociation

Proteolytic digestion

Regulators of complement activation (RCA)

30
Q

What is the role of Factor H? What is the relationship to Factor I? 55

A

Factor H displaces Bb from C3bBb = regulator of C3b production

C3bBb is the C3 Convertase in the alternative pathway

Factor H is a cofactor to Factor I

31
Q

What is the role of Factor I? 55, 59

A

Cleaves both C3b and C4b degrading them

Prevents formation of C3 and C5 Convertases

32
Q

What are the cofactors of Factor I? 55

A

Factor H

MCP

CR1 (C4-BP)

33
Q

What is the first level of control of convertases? 56

A

Decay acceleration

Also, spontaneous inactivation due to diffusion away from site of activation

34
Q

What is the role of C1inh? 57

A

C1 inhibitor

Classic Inhibition:
Binds (2) C1r and (2) C1s inhibiting production of C1qrs = no C2 or C4 cleaving

Lectin Inhibition:
Removes MASP enzyme from MBL complex

35
Q

What’s happening in C1inh deficiency? What disorder does it cause? 58

A

C1qrs not regulated properly resulting in over production of C2a + C2b and C4a + C4b resulting in depletion of C4 and C2

Causes –> Hereditary Angioneurotic Edema (HAE)

36
Q

Within the Lectin pathway, what complex is similar to C1q of the classic pathway? 51

A

MBL-MASPs-Bacteria complex functions the same way as C1q –> they both cleave C4 which leads to cleaving of C2

37
Q

What pathways does DAF (CD55) operate in? 60

A

Decay-accelerating factor is functional in both the:

Alternative pathway: cleaves Bb from C3b

Classical pathway: cleaves C2b from C4b

In both cases = No C3 Convertases!

38
Q

Why is the alternative pathway BAD?

A

BAD

B - factor B
A - alternative pathway
D - factor D

39
Q

Slide 60, right blue boxes

A

(Add)

40
Q

What disease is a result of DAF deficiency? 61

A

PHN - Paroxysmal Nocturnal Hemoglobinuria

41
Q

What happens in Paroxysmal Nocturnal Hemoglobinuria? 61

A

RBC and complement lysis

42
Q

What regulator blocks C9 binding to C5bC678 (MAC)? 62

A

CD59

43
Q

What regulates the fluid phase of the MAC? 62

A

Fluid phase –> C4b67

Vitronectin (S protein) binds fluid phase

If MAC forms it does so in the fluid (not a membrane)

44
Q

What is the main role of C5a? 64

A

An anaphylatoxin that increases the number of complement receptors on cell surfaces

45
Q

How are immune complexes removed from circulation? 65

A

After binding CR1 on RBCs they are transported to the spleen and liver where they are processed and excreted

46
Q

Early in an immune response what is the Ag:Ab ratio? Why is this problematic? 67

A

Large amount of Ags to Abs, not enough Abs to elicit an immune response

47
Q

Go over slide 68

A

(Add)

48
Q

Why is MAC more potent against Erythrocytes, but not other cells? 69

A

Nucleated cells are able to endocytose MACs while RBCs cannot

49
Q

What is C2b synonymous with? 70

A

Prokinin, which can be cleaved by plasmin to yield kinin resulting in edema

50
Q

What does Epstein-Barr virus use as a receptor for attachment to cause disease? 72

A

Binds to CR2 receptor

51
Q

What does Measles virus use as a receptor for attachment to cause disease? 72

A

MCP (CD46) as a receptor

52
Q

What does West Nile virus use as a receptor for attachment to cause disease? 72

A

Is coated by C3b and then uses the CR3 receptor to gain access into a cell

53
Q

Review 76

A

(Add)

HDM - Midterm (9 decks)

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