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complement Flashcards

1
Q

complement given name because

A

complement antigen-antibody

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2
Q

C2 bind with

A

antibody for complement

-clearing of antigen will not happen completely unless complement joins in

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3
Q

antigen-antibody complexes don’t

A

clear everything

need complement!

-we know this because people with complement deficiencies have recurrent infections

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4
Q

Most complement components are synthesized in the

A

liver

-bad liver disease= complement issues

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5
Q

complement biological features

A

Opsonization, Inflammation, Lysis

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6
Q

When complement controlled

A

this is a good thing

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7
Q

When uncontrolled environment

A

ex. Autoimmune disease, will add to inflammatory response

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8
Q

3 pathways

A

Classical, Alternate, lectin

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9
Q

Antibodies that can start the complement cascade

A
  • IgM, IgG, IgA (aggerates– start alternate)
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10
Q

unstable and degrades rapidly

A

complement

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11
Q

At room temp, complement will degrade in a

A

couple hours

also if shake serum degrade
-if acidic or too basic- degrade

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12
Q

One way to destroy complement in lab testing

A

56 degrees for 30 min

-need to use within 30-40 min because will reactivate

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13
Q

Most abundant component of complement

A

C3

value: 70-170
-present in all pathways

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14
Q

2nd most abundant

A

C4

value: 18-45

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15
Q

how is classical activated

A

antigen-antibody complex

-person must be able to mount a response

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16
Q

most complex of 3 pathways

A

classical

-last one to be developed in human

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17
Q

how is classical mainly activated (Ig)

A

IgG and IgM

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18
Q

what else can activate complement on its own?

A

E.coli, rotavirus, high levels of CRP(non specific indicator of inflammation)

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19
Q

3 stages in classical

A

1- Recognition
2- Activation unit
3- Membrane attack unit

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20
Q

in recognition what is needed to be activated

A

2 antibody molecules close enough for the C1q component to bridge and attached to 2 Fc portions

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21
Q

what Ig molecule is better for recognition stage

A

IgM- because pentamer so only need 1 molecule

IgG will need 2 molecules

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22
Q

C1 components

A

C1q, C1r, C1s

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23
Q

component that attaches to antibody molecule

A

C1q

-once attaches activate C1r, then activates C1s

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24
Q

C1r and C1s have

A

enzymatic reactions

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25
what analyte is needed to activate recognition component
calcium
26
activation unit-- C1s will cleave
C4 into C4a and C4b
27
C4b
attaches to cell membrane
28
C4b
goes into fluid spaces -will have mild anaphylactic activity
29
If C4b is not close enough to C1 complex=
will combine with water and rapidly degrade
30
what represents the 1st amplification step
Binding of C4 fragment -Every 1 molecule of C1 activated 30-40 molecules of C4 are spilt
31
C1s will also split
C2 into C2a and C2b
32
C2a
attaches to C4b
33
C2b
goes into fluid spaces
34
c3 convertase
C4b + C2a -most powerful enzyme in the classical pathway
35
C3 convertase splits many molecules of
C3
36
Cleaving of C3 known as
major amplification step
37
C3b attaches to
complex of C2a +C4b
38
C3a
goes into fluid
39
Most phagocytic cells have receptors for
C3b-- makes it one of the most powerful opsins in the immune system
40
C5 convertase
C4b + C2a+ C3b
41
When C5 gets cleaved we
start the membrane attack unit
42
in attack unit C5 gets spilt into
C5b will attach to cell surface
43
C5a
goes off into fluid space -anaphylactic activity
44
once C5 attaches
Other components are not called forth for enzymatic activity, but for what is going on surface membrane
45
C6 and C7 attach to
C5b
46
Once tightly arranged what is called forth
C8 will be called and start to see holes punched into the cell membrane, changed osmotic pressure of the cell causing it to start to leak
47
C9
once get called out, we get complete destruction of the antigen, poke holes and complete cell lysis
48
alternate sometimes called the
properdin pathway -important stabilizing agent of C3 convertase
49
how does alternate pathway begin
C3 -does not depend on antigen-antibody response
50
how can alternate pathway be activated
immunocompromised patient -gram - bacteria (LPS) -fungal elements -tumor cells -virally infected cells -aggregates of IgA
51
where does C3 exist in people
trace amount in everyone's system -relatively unstable -hydrolyze C3 into C3a and C3b
52
hydrolyzes C3 into C3a and C3b= known as
tick over reaction
53
If C3b does not fall onto molecule, it will
degrade
54
In order to remain activate must attach to (alternate)
factor B -will only occur in presence of magnesium ions
55
Once C3b + b attach
factor D comes in and splits factor B into Bb and Ba
56
C3 convertase in the alternate pathway
C3bBb
57
C3bBb enzyme is unstable unless
properdin comes in and stabilizes it -once stable will mimic the classical pathway
58
aka mannose selectin pathway
lectin pathway -believed to be first pathway activated after birth -as get older immune response will not be great
59
lectin pathway is what
antigen-antibody independent
60
how does lectin pathway start
mannose binding lectin (MBL) will attach to mannose found on cell wall of some organisms
61
what does lectin pathway create
inflammatory response and helps immune response
62
Once mannose binding lectin binding starts will activate
C4 C4 will split into C4a and C4b -C2 also spilt
63
what is convertase in lectin pathway
C4bC2a -same as classical pathway
64
how is lectin activated
presence of mannose and certain pathogens
65
what Ig will not activate complement
IgG 4
66
When spilt components go off into fluid spaces
-have biological functions
67
Anaphylactic toxins - increase
vascular permeability -help contract smooth muscles and release of histamine from basophils
68
what has anaphylactic activity
C3a, C4a, C5a -C5a is most potent -all 3 attach to receptors on basophils and allow release of pharmacological agents
69
chemotaxis
directed migration of substances to an area -C5a most potent and can call forth any cell that is needed
70
most potent opsonization in immune system
C3b -becomes a great opsonizer when attaches to cell membrane or antibody -phagocytic cell receptors -RBCs have receptors
71
another great opsonizer
C4a
72
Rapid degradation of complement components
If doesn't fall exactly where needs to fall, will completely disintegrate
72
73
where are soluble/fluid receptors found
circulating in the blood
74
soluble/fluid regulator- C1 inhibitor
-affects classical pathway attach to C1q component and stop any enzymatic activity for C1r and C1s -doesn't prevent C1q from attaching to 2 Fc portions
75
soluble regulator - Factor H
-seen in alternate pathway -will complete with factor B to hook up to C3b
76
what stops the amplification step and no more C3 convertase
C3H
77
Soluble/fluid regulator- Factor I
Ability to cleave C4b and bound C3b into smaller unusable fragments -found in all pathways
78
Soluble/fluid regulator- vitronectin S
Works in all pathways and binds to C5- C7 complex -start of membrane attack unit and prevents the pocking of any holes into a cell
79
where is solid/bound regulators found
host cell membrane -help in deregulation of complement -Prevent bystander lysis of complement
80
what is bystander lysis
Unwanted or mistaken destruction of a cell onto which complement components have fallen
81
what is main preventer of bystander of lysis
DAF- decay accelerating factor (CD55)
82
what does DAF do
-helps decay or breakdown C3 convertase from all pathways of complement
83
Presence of this helps protect cells from bystander lysis
DAF -help determine self vs. non-self
84
self cells will have
DAF
85
non host self
no DAF
86
DAF also known as
CD55
87
manifestation of deficiency of DAF and deficiency of CD59
PNH -more accelerated at night when body temp cools
88
CR1 found on
mainly on neutrophils, macrophages, RBCs, and Eos -binds to C3b and C4b causing dissociation of them so you don't form C5 convertase
89
what does lack of C1 inhibitor do
Overactivation of classical pathway -Increased anaphylactic activity, continued swelling in patient, continued edema, mainly affects respiratory system
90
what else does overactivation of classical pathway cause
hereditary angioedema
91
when hereditary angioedema is measured components will be
decreased -anytime component activated= decreased because cleaved
92
what component of pathway is normal
C1q -because C1 inhibitor does not stop binding
93
lack of C3
Much more prone to pathogenic disease states
94
lack of C2
- initiated by antigen-antibody response -effects any immune response where antigen-antibody interactions are needed -lead to serious infections
95
how is complement measured
CH50
96
what is the CD50 test
hemolytic titration test
97
what is hemolytic titration test
-Measured amount of patient serum required to lyse 50% of a known concentration of antibody coated sheep RBC -add sheep RBC tagged with antibody to serum and should destroy sheep RBC
98
in hemolytic titration when you see 50% lysis what is it called
CH50 ??????? -need to stabilize own units
99
when measuring C3, C4, properdin, nephelometry(light scatter) what are you looking for
-decreases in complement components = means activation of complement -for autoimmune patients we want complement levels to increase = shows working

immuno (5 decks)

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