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Biochem exam 3 > Complement System > Flashcards

Complement System Flashcards

1
Q

What is innate immunity?

A

non-specific immune response
-genetically determined
-include mucous secretion, complement proteins, and certain white blood cells (neutrophils & macrophages)

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2
Q

What is adaptive immunity?

A

specific to antigen/pathogen
-contain lymphocytes and small number of genetically encoded proteins that are able recognize and deactivate specific antigens

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3
Q

What are the two main functions of the complement system?

A

membrane perturbation and inflammation

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4
Q

What is oponsization?

A

it is a part of membrane perturbation
-coats the membrane of pathogens to promote the removal of pathogens
-also leads to the assembly of the membrane attack complex on pathogen membrane that will lead to lysis

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5
Q

How does the complement system enhance inflammatory response?

A

release anaphylatoxins that promote cell activation or migration to an inflammatory site (chemotaxis)

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6
Q

When is the complement system activated?

A

in innate immunity

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7
Q

What are the three ways the complement system can be activated?

A

C3 turnover, natural Abs, and lectins

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8
Q

What does C3 turnover do?

A

engage the alternative pathway

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9
Q

What do Natural Abs do?

A

engage the classical pathway

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10
Q

What do lectins do?

A

bind to carbohydrates on target and engages the lectin pathway

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11
Q

What replaces natural Abs in adaptive immunity?

A

specific Abs

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12
Q

What three immune functions are triggered by the complement system?

A

-phagocytosis
-inflammation
-membrane attack

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13
Q

What has the most important opsonizing activity in phagocytosis?

A

C3b

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14
Q

What are the chemotactically attracting neutrophils and macrophages in inflammation?

A

anaphylatoxins C3a and C5a

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15
Q

What is inflammation?

A

local response to cellular injury that is marked by capillary dilation, leukocytic infiltration, redness, heat, and pain
-serves to eliminate damaged tissue

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16
Q

What is the wheal and flare response?

A

reaction that occurs during type 1 allergic reactions
-swelling produced by release of serum into the tissues (wheal) and redness of skin, resulting from dilation of blood vessels (flare)

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17
Q

What triggers the classical pathway?

A

activation of C1-complex

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18
Q

What is the mannose-binding lectin pathway?

A

homologous to the classical pathway
-uses the opposins: mannose binding lectin and ficolin (NOT C1q)

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19
Q

How does the alternative pathway differ from other pathways?

A

does not rely on pathogen-binding antibodies

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20
Q

is the alternative pathway always activated?

A

yes- at a low level

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21
Q

what is the central component of the complement system?

A

complement fixation

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22
Q

what is complement fixation?

A

C3 cleaved into C3a and C3b
C3b tags bacteria for destruction
C3a recruits phagocytes

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23
Q

What are the three major components of the classical pathway?
(this is hard to word)

A

C1, C2, and C4

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24
Q

What ion is the classical pathway dependent on?

A

magnesium

25
Q

What is the C1 complex?

A

complex of C1q, C1r, and C1s
-heads can bind to constant regions of immunoglobulin molecules or directly to the pathogen surface
-cause conformational change in C1r which cleaves and activates C1s

26
Q

Steps of the classical pathway:

A

-activated C1 cleaves C4 to C4a and C4b, which binds to microbial surface
-C4b binds C2, which is cleaved by C1 to C2a and C2b, forming C4b2a
-C4b2a is a C3 convertase that cleaves C3 to C3a and C3b, which binds to microbial surface or the convertase surface

27
Q

How many C3 molecules can one C4b2a cleave?

A

up to 1000
*amplification effect

28
Q

What are all three pathways (classical, mannose binding, and alternative) dependent on?

A

C3 convertase

29
Q

What are the two serine proteases associated with mannan-binding lectin complex?

A

MASP-1 and 2

30
Q

Who is the hottest in the friend group?

A

Haley

31
Q

Who is the silliest little goose in the friend group?

A

Trick question… Alli and Molly

32
Q

Who always skips class?

A

Dom and Adam

33
Q

Who are the two best roomies ever?

A

Grace and Gracie

34
Q

When the mannan-binding lectin binds to bacterial surfaces, what happens?

A

the serine proteases become activated and then activate the complement system
-cleaves C4 and C2

35
Q

What is C4b2a?

A

C3 convertase

36
Q

What four proteins are involved in the alternative pathway of the complement system?

A

C3, factor B, factor D, and properdin

37
Q

What are the steps of the alternative pathway?

A

-C3b deposited by classical or lectin pathway C3 convertase
-C3b binds to factor B
-bound factor B is cleaved by plasma protease factor D into Ba and Bb
-C3bBb complex is C3 convertase, cleaving many C3 molecules to C3a and C3b

38
Q

What triggers the alternative pathway?

A

covalent binding of C3b to pathogen or cell surface

39
Q

What is Factor B cleaved into?

A

Ba and active protease Bb

40
Q

what are the terminal complement components that form the membrane attack complex?

A

C5b, C6, C7, C8, C9

41
Q

What is the C3 convertase of the alternative pathway?

A

C3bBb

42
Q

What are the steps of the membrane attack complex?

A

-C5b binds to C6 and C7
-C5b67 complex binds to membrane via C7
-C8 binds to the complex and inserts into the cell membrane
-C9 molecules bind to the complex and polymerize
-10-16 molecules of C9 bind to and form a pore in the membrane

need to know: there are pre-made proteins (C9) that allow you to make a pore in cells

43
Q

What does activation of complement cause on the surface of the microorganism?

A

deposition of C3b

44
Q

What binds to C3b to start the process of phagocytosis?

A

CR1 receptor on phagocytes

45
Q

if just C3b is bound to CR1 receptor, does phagocytosis occur?

A

no
*C3b is regulated on whether it will cause phagocytosis or not

46
Q

What causes the activation of the phagocytes?

A

binding to C5a

47
Q

What helps to regulate complement activation?

A

series of proteins that help to protect the host cell from accidental damage

48
Q

what does CD59 do?

A

prevents formation of membrane-attack complex on autologous or allogenic cells

49
Q

What helps to block the creation of excess C3 convertase and C3b?

A

DAF
-blocks the association of Factor B with C3b as well as accelerating dissociation of Bb from C3b

50
Q

what does DAF do?

A

stops formation of new C3b

51
Q

Is disrupting the complement system okay?

A

no, it can cause many different disease

52
Q

What is paroxysmal nocturnal hemoglobinurina?

A

acquired disorder that results in premature death and impair production of blood cells
-RBC, leukocytes, and platelets
-affects both sexes equally
-deficiency in DAF protein

53
Q

What is a treatment for paroxysmal nocturnal hemoglobinurina?

A

therapeutic inhibition of C5
Eculizumab
-humanized recombinant murine monoclonal antibody
-antibody binds to C5 near the cleavage site and prevents its cleavage into C5b and C5a

54
Q

What is atypical hemolytic uremic syndrome?

A

-chronic uncontrolled activation of complement system
-multiple blood clots form throughout the body
-mutation in Factor H, Factor I, or membrane cofactor protein

55
Q

What is hereditary angioedema?

A

-recurrent attacks of severe swelling
-3 types

56
Q

What causes type I hereditary angioedema?

A

mutation in gene that makes C1 inhibitor protein
-deficiency in C1

57
Q

What causes type II hereditary angioedema?

A

mutation in gene that makes C1 inhibitor protein
-atypical C1 protein that is less capable to suppressing activation of complement system

58
Q

What causes type III hereditary angioedema?

A

often due to mutation in Factor XII gene

Biochem exam 3 (10 decks)

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