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Flashcards in CIS - Bowden Deck (53):

What is HERD immunity? 8

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


What are two examples of passive immunization? 10

Snake bite antivenom

Passive transfer of Ig from mother to child


What are two examples of active immunization? 11

Natural exposure to pathogens



Which immunization is immediate and which is delayed? 10

Active immunization --> delayed

Passive immunization --> immediate


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

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



Is IgM produced after birth? 14

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


What are types of live vaccines? 17

Live viruses from different species

Live, attenuated viruses


What are example of inactivated vaccines? 17

Killed/inactivated viruses



Subunit or component of virus


What are two experimental vaccines? 17


Recombinant vector


How can a vaccine be produced against haptens? 21

Through development of conjugated vaccines

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


What's the difference between the "a" and "b" fragments of complement? 35

"a" fragment is smaller (anaphylatoxins)

"b" fragment is larger and usually binds the target


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

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


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

C1qrs continuously cleaves C4

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

C4b2a is our C3 convertase!


Why is C3 such a good opsonizer? 43

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


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

C3 convertase cleavage of many C3


What is the composition of C5 Convertase? 43



What forms the MAC? 44

C5b, C6, C7, C8, C9

First, C5b67 inserts (7 actually in membrane)

C8 associates and attracts C9

C9 forms the pore (10 - 16 copies)


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

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


Why does C3b not bind self-surfaces? 46

Sialic acid on self-surfaces rapidly inactivates C3b


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

C3bBb --> C3 Convertase (alternative pathway)

C3bBb3b --> C5 Convertase (alternative pathway)

Properdin extends the half-life of both of these convertases


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

With the formation of MAC


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

Found in the plasma

From the collectin family, a typeof Ficolin


What cleaves mannose-binding lectin? 50

MBL cleaved by MASPs

MBL-associated serine proteases


Recite a walk through of the Lectin Pathway? 51

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


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

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


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

Neisseria gonorrhoeae

N. Meningitidis


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

C2 deficiency


What disease is caused by C2 deficiency and why? 54

Systemic lupus erythematosis (SLE)

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


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

Binding with dissociation

Proteolytic digestion

Regulators of complement activation (RCA)


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

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


What is the role of Factor I? 55, 59

Cleaves both C3b and C4b degrading them

Prevents formation of C3 and C5 Convertases


What are the cofactors of Factor I? 55

Factor H


CR1 (C4-BP)


What is the first level of control of convertases? 56

Decay acceleration

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


What is the role of C1inh? 57

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


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

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)


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

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


What pathways does DAF (CD55) operate in? 60

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!


Why is the alternative pathway BAD?


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


Slide 60, right blue boxes



What disease is a result of DAF deficiency? 61

PHN - Paroxysmal Nocturnal Hemoglobinuria


What happens in Paroxysmal Nocturnal Hemoglobinuria? 61

RBC and complement lysis


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



What regulates the fluid phase of the MAC? 62

Fluid phase --> C4b67

Vitronectin (S protein) binds fluid phase

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


What is the main role of C5a? 64

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


How are immune complexes removed from circulation? 65

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


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

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


Go over slide 68



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

Nucleated cells are able to endocytose MACs while RBCs cannot


What is C2b synonymous with? 70

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


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

Binds to CR2 receptor


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

MCP (CD46) as a receptor


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

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


Review 76