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Spring 2022 > BIOL 435 Ch. 5 Part Two (The Complement System) > Flashcards

BIOL 435 Ch. 5 Part Two (The Complement System) Flashcards

1
Q

3 classes of C’ activity

A
  1. Innate defense against infection
  2. Interface between innate and adaptive immunity
  3. C’ in the contraction phase of the immune response
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2
Q

C’ receptors

A

-connect complement-tagged pathogens to effector cells

>receptors on host cells allow for discrete and differentiated responses

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3
Q

C’ receptors examples

A
  • CR1
  • CR2 (CD21)
  • C3aR
  • C5aR
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4
Q

CR1

A
  • on leukocytes and erythrocytes

- recognize C3b

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5
Q

CR1 on leukocytes

A

-helps bring immune complexes (Ag/Ab) to the liver for clearance by pathogens

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6
Q

CR1 on phagocytes

A

-helps bind complement-coated bacteria to enhance ingestion and destruction

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7
Q

CR1 on B-cells

A

-helps bind to complement coated Ag

>enhances ingestion for processing and presentation to helper T-cells

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8
Q

CR1 on B-cell binds C3b on pathogen

A

-C3b cleaved by factor 1= iC3b and C3d
-C3d helps activate B-cell
>allows less exposure needed to be activated

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9
Q

C3aR/C5aR

A
  • on granulocytes
  • GPCR
  • stimulate release of proinflammatory cytokines and granule components from basophils, eosinophils and neutrophils
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10
Q

C’ enhances host defense against infection

A
  1. MAC-induced cell death
  2. Connect C’ tagged pathogens to effector cells
  3. Promote inflammation
  4. Promote opsonization
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11
Q

promotion of opsonization

A
  • opsonized microbes easier to ingest/destroy

- opsonized immune complexes easier to clear

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12
Q

C’ mediates interface between innate and adaptive

A
  1. Enhance antigen uptake
  2. Enhance B-cell response
  3. Lyse immature T-cells with low sialic acid
  4. Bind C3a, C5a and C3b
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13
Q

enhane Ag uptake

A

-of Ag bound to MBL, C1q, C3b, and C4b that binds receptors on APCs

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14
Q

enhance B-cell response

A

-by increasing avidity of B-cell binding to C’-bound Ag

>triggers adaptive at a lower rate

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15
Q

sialic acid

A

-a CHO that increases in concentration as a protective coating on maturing T-cells
>keeps immature T-cells from being released to early

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16
Q

binding of C3a, C5a and C3b

A
  • to their receptors on mature T-cells

- facilitates their growth, differentiation, and survival

17
Q

C’ aids in contraction phase of immune response

A
  • disposal of apoptotic cells and bodies as lympocytes are no longer required
  • removal of immune complexes formed during response
  • these avoid damaging inflammation induction in the absence of Ag following clearance of an infection
18
Q

C’ activity passively regulated by

A
  1. Protein stability
  2. Cell-surface composition
    >self-cells
19
Q

protein stability

A

-short half-life of C3 convertase unless stabilized by properdin

20
Q

self-cells

A

-possess different CHO structures that are more effectively bound by inhibitory enzymes (fluid-phase proteases)
>these more readily inactivate C3b through hydrolysis, protecting self cells

21
Q

C1INH

A

-C1 inhibitor
-promotes dissociation of serine proteases
-causes C1r2s2 to dissociate from C1q
>no further clevage of C4 or C2 is possible
-inhibits initiation of classical and lectin C’ pathway

22
Q

decay accelerating factors (DAF)

A

-promote decay of C3 convertases (C4b2a on surface of host cells)
-several different proteins wiht similar activities
>DAF (CD55)
>Factor H

23
Q

Factor H

A

-binds negatively charged cell surface sialic acid and heparin (molecules unique to eukaryotic cell surfaces)

24
Q

Factor 1

A
  • degrades C3b and C4b
  • soluble, constitutively active serine protease
  • cleaves membrane-associated C3b and C4b into inactive fragments
25
Q

protectin

A

-CD59
-inhibits the MAC attack
-binds C3b678 complexes deposited by host cells
>prevents insertion into PM
>blocks C9 recruitment

26
Q

vitronectin

A
  • soluble C’ S protein

- binds fluid phase C5b67 to prevent insertion into hostcell PM

27
Q

carboxypeptidases

A

-can inactivate the anaphylatoxins (C3a, C5a)
-remove arginine resides
>creates des-Arg inactive forms
>helps shut down unnecessary or dangerous chemotactic and inflammatoion induction

28
Q

genetic deficiences

A
  • described for each C’ components

- outcomes vary

29
Q

C1q, C1r, C1s, C4 or C2 deficiency

A
  • immune complex disorders due to inadequate immune complex clearance
  • anything before/above C3b=problem!
30
Q

MBL deficiency

A

-may exhibit greater frequency of infections by encapsulated bacteria due to inefficient opsonization and phagocytosis

31
Q

microbial C’ evasion strategies

A
  1. Interfere with first step of Ig-mediated C’ activation
  2. Microbial proteins may bind and inactivate C’ proteins
  3. Microbial proteases destroy C’ proteins
  4. Mimic or bind C’ regulatory proteins

Spring 2022 (54 decks)

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