2 Hour Surprise Complement Lecture Flashcards

(52 cards)

1
Q

Immunization

A

Ag stimulus that stimulus specific adaptive immune response that can be recalled during subsequent infections
Passive - Ab/antiserum only
Active - intro Ag that induces adaptive immune response

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2
Q

Herd immunity

A

Immunity acquired when a critical number of individuals in a population are vaccinated

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3
Q

Considerations for immunization schedule

A

Timing of exposure
Immunological maturity of child
Passively transferred Ab that may interfere with immune response of vaccine
Interference

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4
Q

Passively transferred maternal IgG is completely degraded

A

At 9 months of age

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5
Q

Criteria for effective vaccine (only indicated item)

A

Must induce protective T cells
Some pathogens, particularly intracellular, are more effectively dealt with by cell-mediated responses
Also need T cells to activate B cells for Ab production

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6
Q

Inactivated vaccines contain

A

Killed/ inactivated viruses
Subunits or components
Toxoid
Conjugated Ag

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7
Q

Adjuvants

A

Increase vaccine efficacy
Bacterial components or media that prolongs exposure or induces mild inflammation to attract phagocytes (increases chance that Ag will be picked up and presented)

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8
Q

Conjugate vaccines

A

Capsular polysaccharides from pathogenic bacteria elicit a t independent response
Must conjugate the vaccines by linking to a polysaccharide to Ag or toxoid to form an immunogen (t-dependent Ag)

HiB vaccine

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9
Q

Immunological tolerance

A

Unresponsiveness of adaptive immune system to Ag as a result of inactivation or death of Ag-specific lymphocytes, induced by exposure to the Ag

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10
Q

Factors that promote immune tolerance

A
Soluble, aggregate free, simple small molecules
Improper processing 
Oral/IV presentation 
Age (too young or too old) 
Dose (too large or small)
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11
Q

Characteristics that promote adaptive immune response

A
Large, aggregated complex molecules 
Proper processing 
Subcutaneous or IM exposure 
Intermediate dose 
not young af or old af
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12
Q

Functions of complement

A
Triggering, amplification of inflammation 
Attraction of phagocytes by chemotaxis 
Clearance of immune complexes 
Cellular activation 
Direct microbial killing
Development of humoral response
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13
Q

Classical pathway is activated by

A

Ab-Ag complex stimulates C1 binding

Either IgG or IgM (must bind multiple globular domains of C1q in order to activate)

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14
Q

Alternative pathway activated by

A

Spontaneous lysis of C3

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15
Q

Lectin pathway initiated by

A

MBL binding lectin and recruiting MASP1 + MASP2

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16
Q

C1qrs can be inhibited by

A

C1 inhibitor

Binds C1r and C1s to prevent cleave of C4 and C2

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17
Q

C3 convertase classical pathway consists of

A

C4b2a

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18
Q

C5 convertase classical pathway consists of

A

C4b2a3b

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19
Q

Inserts into membrane and forms small pore

A

C4b67

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20
Q

Recruits 10-16 copies of C9

A

C8

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21
Q

Host cells protect themselves from spontaneous lysis of C3 by expressing high levels of what on their cell surface

22
Q

Factor D

A

Cleaves factor B –> Bb and Ba

23
Q

Binds C3bBb and C3bBb3b and prevents increases half-life

24
Q

Alternative C3 convertase

25
Alternative C5 convertase
C3bBb3b
26
Binds N-acetylglucosamine on bacterial cell wall to induce autocleavage of MASP1 and MASP2
Ficolin
27
Deficiency resulting in: High degree of SLE from failure to clear circulatory immune complexes - deposits on endothelial cells and activates alternative complement, local inflammation
C2 deficiency
28
Deficiencies in Factor H and Factor I mimic
C3 deficiencies - unregulated C3b generation exhausts C3 from serum
29
Deficiency results in increased susceptibility to Neisseria gonorrhoeae and N. meningitidis
MAC deficiencies (C5-C9)
30
Factor I
Cleaves C3b and C4b Cofactors: Factor H, MCP, C4BP, CR1 SERINE PROTEASE
31
Factor H
Binds C3b and displaces Bb | Also serves as a cofactor for Factor I cleavage of C3b
32
C4BP
C4 binding protein - binds C3b and displaces C2 | Cofactor for Factor I cleavage of C4b
33
DAF functions in a similar capacity as what two RCAs?
``` Factor H (alternative pathway) C4BP (classical pathway) ```
34
MCP
Also known as CD46 | Cofactor for Factor I cleavage of C3b and C4b
35
DAF
Displaces C2b from C4b (classical) Displaces Bb from C3b (alternative) Aka inactivates the C3 convertases
36
CD59
Blocks C9 binding and prevents formation of MAC
37
Vibronectin
S protein - prevents C5b67 from penetrating (heh) membrane
38
Hereditary Angioneurotic Edema
C1 inhibitor deficiency Swelling attacks from physical trauma/emotional stress Affects extremities, face, GI tract Treat with androgens (increase transcription of C1 inhibitors)
39
Paroxysmal nocturnal hemoglobinuria
Deficient DAF Hemolytic disorder with spontaneous episodes of RBC lysis, leukocytes, platelets sensitive to complement Treat with EPO
40
Type III Hypersensitivity
Little Ab and excess Ag will lead to small immune complexes that are not cleared from circulation because they do not fix complement --> local inflammation --> basophils degranulation, platelet aggregation --> increase vascular permeability --> complex deposition --> attract neutrophils who further mess it up ==> increased Bp and vascular turbulence
41
Biological functions of complement
``` Opsonization (C3b, and a little C4b) Waste management (C3b binds CR1 of RBCs to transport Immune complexes to spleen/liver) Cell lysis (mac) Inflammatory mediators (anaphylatoxins C3a, C5a, C5b67) ```
42
Prokinin
Also known as C2b - cleaved by plasmin to yield kinin --> edema
43
Epstein Barr virus abuses complement to gain entry into cells by
Using CR2 as a receptor for attachment
44
Measles utilizes the complement system to infect cells by
Using MCP (CD46) as a receptor
45
West Nile hijacks complement machinery by
Coating viral particles in C3b to gain entry into cells by CR3
46
Neisseria meningitidis escapes complement degradation by
Expressing protein on its cell surface that block the formation of convertases
47
CH50 assay tests for
Test ability of patients blood to perform Complement mediated hemolysis
48
Classical deficiency
Increases risk of developing immune complex diseases like SLE
49
MBL deficiency
Increases risk of infection by yeast sacchromyces cerevisiae and encapsulated bacteria
50
Alternative pathway deficiency
Decreases opsonization activity and increases risk of infection by encapsulated bacteria
51
C3 deficiency
``` Leads to Defective opsonization Defective leukocyte chemotaxis Decreased bactericidal killing activity (no MAC) Also indicated in immune complex disease ```
52
MAC deficiency
Increased risk of infection to N. meningitidis