5 – Innate Immunity II Flashcards

(51 cards)

1
Q

what is th Complement system

A

Group of soluble proteins that cooperate with both innate & adaptive immune systems
To eliminate: Pathogens, Dying cells, Immune complexes from the body

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2
Q

Complement systems are mostly:

A

-Mostly Proteases in blood/other fluids
Protease: enzyme that performs proteolysis – break down proteins

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3
Q

most complement are called:

A

C follow by number

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4
Q

other compliement are called

A

factor follow by capital letter

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5
Q

Complement proteins are mostly produced by

A

Liver

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6
Q

complement proteins creates a cascade, what is this?

A

Set off a chain reaction – help to clear pathogen

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7
Q

key mechanisms of action (3)

A

-Increase vascular permeability (vasodilate) & chemotaxis (inflammation)
-Destroy pathogen cell membranes (poke holes)
-Increase recognition of pathogen & facilitate phagocytosis – opsonization

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8
Q

what is Opsonization

A

-coating of surface of a pathogen by antibody and/or complement that makes it more easily ingested by phagocytes
-To make pathogen tastier for phagocytes

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9
Q

what is phagocytosis

A

internalization of matter by cells by engulfment, in which cell membrane surrounds the material – form an intracellular vesicle (phagosome) containing ingested material

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10
Q

what are inactive complements called and what do they do

A

inactive pro-proteases
-they circulate and have nothing to do

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11
Q

activated in which 3 pathways

A

-classical
-lectin
-alternative

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12
Q

pathway lead to a cascade of effect: what happens in this cascade?

A

all 3 pathways generate C3 convertase (cleave C3 -> C3a +C3b)

Proteolytic cleavage generates 2 fragments

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13
Q

proteolytic cleavage generates 2 active fragments they are:

A

-1 small
Letter “a” after name
C5a
With specific function
-1 large
Letter “b” after name
C5b
With proteolytic activity on new substrate

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14
Q

Complement nomenclature: C4b binds with C2a

A

C4b2a

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15
Q

Complement nomenclature: C3b binds with Bb (factor)

A

C3bBb

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16
Q

C4b2a and C3bBb are known as:

A

C3 converts

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17
Q

what does C3 convertase do?

A

(cleave C3 -> C3a +C3b)

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18
Q

complement proteins are only active when

A

when they are cleaved with protease

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19
Q

All 3 pathways generate

A

C3 converts

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20
Q

what are he 3 main outcomes from activation of pathways

A

-Inflammation
-opsonization
-MAC formation

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21
Q

Lectin pathway is Triggered by: give 2 examples

A

-soluble proteins – lectins (PRR that circulate in blood)
-Not membrane-bound PRRs
Mannose-binding lectin (MBL)
Ficolin

22
Q

during infection, lectin:

A

Expression of lectin = increas

23
Q

Lectin PRRs can:

A

-PRRs can bind the surface of pathogens
-Trigger signaling cascade on pathogen surface
-C3 convertase generated (C4b2a)
-C3 cleaved -> C3a + C3b

24
Q

initiator of classical pathway

25
what can C1q do:
-C1q binds pathogen surface -Can bind pathogen directly -Can bind antibodies bound to pathogen surface
26
which path way connect adaptive and innate immunity
Classical pathway: -C1q can bind to antibodies bounf to pathogen surface (geenrated by activated B cells -adaptive immunity)
27
what happens once C1q is bound:
-Triggers signaling cascade on pathogen surface C3 convertase generated (C4b2a) C3 cleaved -> C3a +C3b
28
Classical & lectin pathway result in generation of which C3 converts
C4b2a
29
C3a involved in
enhancing inflammation
30
C3b involed in:
opsonization & C5 convertase -> C5a + C5b
31
1st alternative pathway
-Once C3b produces by lectin/classical pathway activation -Amplification loop for C3b formation (depose more C3b on pathogen) -Require factor B & protease factor D -Factor D cleave factor B -> Ba +Bb -makes C3bBb - C3 convertase
32
what does alternative pathway make:
C3bBb - C3 convertase
33
2nd alternative pathway
-When high concentration of C3 (liver produced - inactive) --> undergo spontaneous hydrolysis -Involves factors B & D -makes C3bBb
34
whats different from alternaitve pathway C3 convertase (C3bBb) and classical/lectin pathway C3 convertase (C4b2a)
C3bBb is very unstable
35
how to stabilize C3bBb
-Stabilized by factor P (properdin) secreted by neutrophils -Properdin stabilize C3 convertase as it can bind to some microbial surfaces
36
pathogens are mainly ... for the complement system. why?
extracellular -everything is deposited on the pathigen surface --> phagocytosis -phagocytosis are for extracellular bacteria -MAC formation-pores forming on cell's surface
37
complement system act mainly on:
exracellular pathogens: -phagocytosis -MAC formation
38
Downstream effect of C3 convertase cleaving:
Inflammation Increase phagocytosis Pathogen lysis
39
downstream effect: inflmmation
-Additional signaling = cleavage of other complement molecules -C3a & C5a recruit phagocytes & promote inflammation
40
what happens too much inflammation:
-If present in large amount – C3a & C5a --> anaphylactic shock
41
what happens when promoting inflammation?
-Complement receptors connect complement tagged pathogens to effector cells -C3aR/C5aR on granulocytes -Stimulate release of proinflammatory cytokines & granule components from basophils/eosinophils/neutrophils/mast cells
42
Downstream effect: Increase phagocytosis
-Phagocytes have receptor on C3b -Opsonization of pathogen -Opsonization can happen via complement deposition and/or antibodies (phagocytes also have receptors for antibodies)
43
downstream effect: Pathogen lysis
-Additional complement factors create MAC (membrane-attack complex) -> cell lysis -C5b (directly) & C3b (indirectly) involved -Cascade leading to formation of MAC –
44
Negative regulation of Complement activation: who is responsible
-Complement-regulatory proteins in plasma or cell surfaces
45
Negative regulation of Complement activation: what happens
-prevent complement activation from proceeding normal/basal conditions -Prevent appearance of C3 convertase -Promote disappearance of C3 convertase
46
2 C3 convertase and what do they do
C4b2a & C3bBb cleaves C3 to C3a & C3b
47
C3b role
involved in opsonization & C5 convertase
48
what is C5 convertase involved in
indirectly involved in MAC
49
C3a role
inflammation
50
C5b role
MAC
51
C5a
inflammation